Volume 8, Issue 11

Halade GV, Kain V, Black LM, Prabhu SD, Ingle KA, . Aging dysregulates D- and E-series resolvins to modulate cardiosplenic and cardiorenal network following myocardial infarction. . 8:2611-2634. https://doi.org/10.18632/aging.101077

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Halade, Ganesh V. 
                AU  - Kain, Vasundhara 
                AU  - Black, Laurence M. 
                AU  - Prabhu, Sumanth D. 
                AU  - Ingle, Kevin A. 
                TI  - Aging dysregulates D- and E-series resolvins to modulate cardiosplenic and cardiorenal network following myocardial infarction
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101077
                DO  - 10.18632/aging.101077
                SP  - 2611
                EP  - 2634
                PY  - 
                AB  - Post-myocardial infarction (MI), overactive inflammation is the hallmark of aging, however, the mechanism is unclear. We hypothesized that excess influx of omega 6 fatty acids may impair resolution, thus impacting the cardiosplenic and cardiorenal network post-MI. Young and aging mice were fed on standard lab chow (LC) and excess fatty acid (safflower oil; SO)-enriched diet for 2 months and were then subjected to MI surgery. Despite similar infarct areas and left ventricle (LV) dysfunction post-MI, splenic mass spectrometry data revealed higher levels of arachidonic acid (AA) derived pro-inflammatory metabolites in young-SO, but minimal formation of docosanoids, D- and E- series resolvins in SO-fed aged mice. The aged mice receiving excess intake of fatty acids exhibit; 1) decreased lipoxygenases (5-,12-, and 15) in the infarcted LV; 2) lower levels of 14HDHA, RvD1, RvD5, protectin D1, 7(S)maresin1, 8-,11-,18-HEPE and RvE3 with high levels of tetranor-12-HETEs; 3) dual population of macrophages (CD11blow/F480high and CD11bhigh/F480high) with increased pro-inflammatory (CD11bp+F4/80+Ly6Chi) phenotype and; 4) increased kidney injury marker NGAL with increased expression of TNF-α and IL-1β indicating MI-induced non-resolving response compared with LC-group. Thus, excess fatty acid intake magnifies the post-MI chemokine signaling and inflames the cardiosplenic and cardiorenal network towards a non-resolving microenvironment in aging.
                ER  -

Click to copy this citation from the text box above or download the citation:

Distinct patterns of simple sequence repeats and GC distribution in intragenic and intergenic regions of primate genomes

Wen-Hua Qi, Chao-chao Yan, Wu-Jiao Li, Xue-Mei Jiang, Guang-Zhou Li, Xiu-Yue Zhang, Ting-Zhang Hu, Jing Li, Bi-Song Yue,

https://doi.org/10.18632/aging.101025 pp 2635—2654

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Qi W, Yan C, Li W, Jiang X, Li G, Zhang X, Hu T, Li J, Yue B, . Distinct patterns of simple sequence repeats and GC distribution in intragenic and intergenic regions of primate genomes. . 8:2635-2654. https://doi.org/10.18632/aging.101025

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Qi, Wen-Hua 
                AU  - Yan, Chao-chao 
                AU  - Li, Wu-Jiao 
                AU  - Jiang, Xue-Mei 
                AU  - Li, Guang-Zhou 
                AU  - Zhang, Xiu-Yue 
                AU  - Hu, Ting-Zhang 
                AU  - Li, Jing 
                AU  - Yue, Bi-Song 
                TI  - Distinct patterns of simple sequence repeats and GC distribution in intragenic and intergenic regions of primate genomes
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101025
                DO  - 10.18632/aging.101025
                SP  - 2635
                EP  - 2654
                PY  - 
                AB  - As the first systematic examination of simple sequence repeats (SSRs) and guanine-cytosine (GC) distribution in intragenic and intergenic regions of ten primates, our study showed that SSRs and GC displayed nonrandom distribution for both intragenic and intergenic regions, suggesting that they have potential roles in transcriptional or translational regulation. Our results suggest that the majority of SSRs are distributed in non-coding regions, such as the introns, TEs, and intergenic regions. In these primates, trinucleotide perfect (P) SSRs were the most abundant repeats type in the 5'UTRs and CDSs, whereas, mononucleotide P-SSRs were the most in the intron, 3'UTRs, TEs, and intergenic regions. The GC-contents varied greatly among different intragenic and intergenic regions: 5'UTRs &gt; CDSs &gt; 3'UTRs &gt; TEs &gt; introns &gt; intergenic regions, and high GC-content was frequently distributed in exon-rich regions. Our results also showed that in the same intragenic and intergenic regions, the distribution of GC-contents were great similarity in the different primates. Tri- and hexanucleotide P-SSRs had the most GC-contents in the 5'UTRs and CDSs, whereas mononucleotide P-SSRs had the least GC-contents in the six genomic regions of these primates. The most frequent motifs for different length varied obviously with the different genomic regions.
                ER  -

Click to copy this citation from the text box above or download the citation:

Ischemic stroke patients are biologically older than their chronological age

Carolina Soriano-Tárraga, Eva Giralt-Steinhauer, Marina Mola-Caminal, Rosa M. Vivanco-Hidalgo, Angel Ois, Ana Rodríguez-Campello, Elisa Cuadrado-Godia, Sergi Sayols-Baixeras, Roberto Elosua, Jaume Roquer, Jordi Jiménez-Conde,

https://doi.org/10.18632/aging.101028 pp 2655—2666

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Soriano-Tárraga C, Giralt-Steinhauer E, Mola-Caminal M, Vivanco-Hidalgo RM, Ois A, Rodríguez-Campello A, Cuadrado-Godia E, Sayols-Baixeras S, Elosua R, Roquer J, Jiménez-Conde J, . Ischemic stroke patients are biologically older than their chronological age. . 8:2655-2666. https://doi.org/10.18632/aging.101028

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Soriano-Tárraga, Carolina 
                AU  - Giralt-Steinhauer, Eva 
                AU  - Mola-Caminal, Marina 
                AU  - Vivanco-Hidalgo, Rosa M.
                AU  - Ois, Angel 
                AU  - Rodríguez-Campello, Ana 
                AU  - Cuadrado-Godia, Elisa 
                AU  - Sayols-Baixeras, Sergi 
                AU  - Elosua, Roberto 
                AU  - Roquer, Jaume 
                AU  - Jiménez-Conde, Jordi 
                TI  - Ischemic stroke patients are biologically older than their chronological age
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101028
                DO  - 10.18632/aging.101028
                SP  - 2655
                EP  - 2666
                PY  - 
                AB  - Ischemic stroke is associated with aging. It is possible to predict chronological age by measuring age-related changes in DNA methylation from multiple CpG sites across the genome, known as biological age. The difference between biological age and actual chronological age would indicate an individual’s level of aging. Our aim was to determine the biological age of ischemic stroke patients and compare their aging with controls of the same chronological age. A total of 123 individuals, 41 controls and 82 patients with ischemic stroke were paired by chronological age, ranging from 39 to 82 years. Illumina HumanMethylation450 BeadChip array was used to measure DNA methylation in CpG sites in both groups, and biological age was estimated using methylation values of specific CpGs. Ischemic stroke patients were biologically an average 2.5 years older than healthy controls (p-value=0.010). Stratified by age tertiles, younger stroke patients (≤57 years old) were biologically older than controls (OR=1.19; 95%CI 1.00-1.41, p-value=0.046). The older groups showed no biological age differences between cases and controls, but were close to reaching the significance level. Ischemic stroke patients are biologically older than controls. Biological age should be considered as a potential new biomarker of stroke risk.
                ER  -

Click to copy this citation from the text box above or download the citation:

The progeroid gene BubR1 regulates axon myelination and motor function

Chan-Il Choi, Ki Hyun Yoo, Syed Mohammed Qasim Hussaini, Byeong Tak Jeon, John Welby, Haiyun Gan, Isobel A. Scarisbrick, Zhiguo Zhang, Darren J. Baker, Jan M. van Deursen, Moses Rodriguez, Mi-Hyeon Jang,

https://doi.org/10.18632/aging.101032 pp 2667—2688

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Choi C, Yoo KH, Hussaini SM, Jeon BT, Welby J, Gan H, Scarisbrick IA, Zhang Z, Baker DJ, van Deursen JM, Rodriguez M, Jang M, . The progeroid gene BubR1 regulates axon myelination and motor function. . 8:2667-2688. https://doi.org/10.18632/aging.101032

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Choi, Chan-Il 
                AU  - Yoo, Ki Hyun
                AU  - Hussaini, Syed Mohammed Qasim
                AU  - Jeon, Byeong Tak
                AU  - Welby, John 
                AU  - Gan, Haiyun 
                AU  - Scarisbrick, Isobel A.
                AU  - Zhang, Zhiguo 
                AU  - Baker, Darren J.
                AU  - van Deursen, Jan M.
                AU  - Rodriguez, Moses 
                AU  - Jang, Mi-Hyeon 
                TI  - The progeroid gene BubR1 regulates axon myelination and motor function
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101032
                DO  - 10.18632/aging.101032
                SP  - 2667
                EP  - 2688
                PY  - 
                AB  - Myelination, the process by which oligodendrocytes form the myelin sheath around axons, is key to axonal signal transduction and related motor function in the central nervous system (CNS). Aging is characterized by degenerative changes in the myelin sheath, although the molecular underpinnings of normal and aberrant myelination remain incompletely understood. Here we report that axon myelination and related motor function are dependent on BubR1, a mitotic checkpoint protein that has been linked to progeroid phenotypes when expressed at low levels and healthy lifespan when overabundant. We found that oligodendrocyte progenitor cell proliferation and oligodendrocyte density is markedly reduced in mutant mice with low amounts of BubR1 (BubR1H/H mice), causing axonal hypomyelination in both brain and spinal cord. Expression of essential myelin-related genes such as MBP and PLP1 was significantly reduced in these tissues. Consistent with defective myelination, BubR1H/H mice exhibited various motor deficits, including impaired motor strength, coordination, and balance, irregular gait patterns and reduced locomotor activity. Collectively, these data suggest that BubR1 is a key determinant of oligodendrocyte production and function and provide a molecular entry point to understand age-related degenerative changes in axon myelination.
                ER  -

Click to copy this citation from the text box above or download the citation:

Investigating the associations between adiposity, life course overweight trajectories, and telomere length

Wahyu Wulaningsih, Johnathan Watkins, Tetsuya Matsuguchi, Rebecca Hardy,

https://doi.org/10.18632/aging.101036 pp 2689—2701

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wulaningsih W, Watkins J, Matsuguchi T, Hardy R, . Investigating the associations between adiposity, life course overweight trajectories, and telomere length. . 8:2689-2701. https://doi.org/10.18632/aging.101036

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wulaningsih, Wahyu 
                AU  - Watkins, Johnathan 
                AU  - Matsuguchi, Tetsuya 
                AU  - Hardy, Rebecca 
                TI  - Investigating the associations between adiposity, life course overweight trajectories, and telomere length
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101036
                DO  - 10.18632/aging.101036
                SP  - 2689
                EP  - 2701
                PY  - 
                AB  - Obesity may accelerate ageing through chronic inflammation. To further examine this association, we assessed current adiposity, adiposity at early adulthood and life course overweight trajectories in relation to leukocyte telomere length (LTL). We included a total of 7,008 nationally representative U.S. residents and collected information on objectively measured body mass index (BMI), waist circumference and percent body fat. BMI at age 25 and overweight trajectories were assessed using self-reported history. Leukocyte telomere length (LTL) relative to a standard DNA reference (T/S ratio) was quantified by polymerase chain reaction (PCR). Linear regression models were used to examine the difference in LTL across adiposity measures at examination, BMI at age 25, and overweight trajectories. A 0.2% decrease in telomere length (95% CI: -0.3 to -0.07%) was observed for every kg/m2 increase in BMI, whereas a unit increase in waist circumference (cm) and percent body fat contributed to a 0.09% and 0.01% decrease in LTL, respectively. Higher BMI and being obese at age 25 contributed to lower LTL at older ages. Associations between weight loss through life course and LTL were observed, which further marked the importance of life course adiposity dynamics as a determinant of ageing.
                ER  -

Click to copy this citation from the text box above or download the citation:

Mutational load of the mitochondrial genome predicts pathological features and biochemical recurrence in prostate cancer

Anton M.F. Kalsbeek, Eva F.K. Chan, Judith Grogan, Desiree C. Petersen, Weerachai Jaratlerdsiri, Ruta Gupta, Ruth J. Lyons, Anne-Maree Haynes, Lisa G. Horvath, James G. Kench, Phillip D. Stricker, Vanessa M. Hayes,

https://doi.org/10.18632/aging.101044 pp 2702—2712

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Kalsbeek AM, Chan EF, Grogan J, Petersen DC, Jaratlerdsiri W, Gupta R, Lyons RJ, Haynes A, Horvath LG, Kench JG, Stricker PD, Hayes VM, . Mutational load of the mitochondrial genome predicts pathological features and biochemical recurrence in prostate cancer. . 8:2702-2712. https://doi.org/10.18632/aging.101044

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Kalsbeek, Anton M.F. 
                AU  - Chan, Eva F.K. 
                AU  - Grogan, Judith 
                AU  - Petersen, Desiree C. 
                AU  - Jaratlerdsiri, Weerachai 
                AU  - Gupta, Ruta 
                AU  - Lyons, Ruth J. 
                AU  - Haynes, Anne-Maree 
                AU  - Horvath, Lisa G. 
                AU  - Kench, James G. 
                AU  - Stricker, Phillip D. 
                AU  - Hayes, Vanessa M. 
                TI  - Mutational load of the mitochondrial genome predicts pathological features and biochemical recurrence in prostate cancer
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101044
                DO  - 10.18632/aging.101044
                SP  - 2702
                EP  - 2712
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Kalsbeek, Anton M.F. 
                AU  - Chan, Eva F.K. 
                AU  - Grogan, Judith 
                AU  - Petersen, Desiree C. 
                AU  - Jaratlerdsiri, Weerachai 
                AU  - Gupta, Ruta 
                AU  - Lyons, Ruth J. 
                AU  - Haynes, Anne-Maree 
                AU  - Horvath, Lisa G. 
                AU  - Kench, James G. 
                AU  - Stricker, Phillip D. 
                AU  - Hayes, Vanessa M. 
                TI  - Mutational load of the mitochondrial genome predicts pathological features and biochemical recurrence in prostate cancer
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101044
                DO  - 10.18632/aging.101044
                SP  - 2702
                EP  - 2712
                PY  - 
                AB  - Prostate cancer management is complicated by extreme disease heterogeneity, which is further limited by availability of prognostic biomarkers. Recognition of prostate cancer as a genetic disease has prompted a focus on the nuclear genome for biomarker discovery, with little attention given to the mitochondrial genome. While it is evident that mitochondrial DNA (mtDNA) mutations are acquired during prostate tumorigenesis, no study has evaluated the prognostic value of mtDNA variation. Here we used next-generation sequencing to interrogate the mitochondrial genomes from prostate tissue biopsies and matched blood of 115 men having undergone a radical prostatectomy for which there was a mean of 107 months clinical follow-up. We identified 74 unique prostate cancer specific somatic mtDNA variants in 50 patients, providing significant expansion to the growing catalog of prostate cancer mtDNA mutations. While no single variant or variant cluster showed recurrence across multiple patients, we observe a significant positive correlation between the total burden of acquired mtDNA variation and elevated Gleason Score at diagnosis and biochemical relapse. We add to accumulating evidence that total acquired genomic burden, rather than specific mtDNA mutations, has diagnostic value. This is the first study to demonstrate the prognostic potential of mtDNA mutational burden in prostate cancer.
                ER  -

Click to copy this citation from the text box above or download the citation:

An antioxidant specifically targeting mitochondria delays progression of Alzheimer’s disease-like pathology

Natalia A. Stefanova, Natalia A. Muraleva, Kseniya Yi. Maksimova, Ekaterina A. Rudnitskaya, Elena Kiseleva, Darya V. Telegina, Nataliya G. Kolosova,

https://doi.org/10.18632/aging.101054 pp 2713—2733

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Stefanova NA, Muraleva NA, Maksimova KY, Rudnitskaya EA, Kiseleva E, Telegina DV, Kolosova NG, . An antioxidant specifically targeting mitochondria delays progression of Alzheimer’s disease-like pathology. . 8:2713-2733. https://doi.org/10.18632/aging.101054

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Stefanova, Natalia A.
                AU  - Muraleva, Natalia A.
                AU  - Maksimova, Kseniya Yi.
                AU  - Rudnitskaya, Ekaterina A.
                AU  - Kiseleva, Elena 
                AU  - Telegina, Darya V.
                AU  - Kolosova, Nataliya G.
                TI  - An antioxidant specifically targeting mitochondria delays progression of Alzheimer’s disease-like pathology
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101054
                DO  - 10.18632/aging.101054
                SP  - 2713
                EP  - 2733
                PY  - 
                AB  - Mitochondrial aberrations are observed in human Alzheimer’s disease (AD) and in medical conditions that increase the risk of this disorder, suggesting that mitochondrial dysfunction may contribute to pathophysiology of AD. Here, using OXYS rats that simulate key characteristics of sporadic AD, we set out to determine the role of mitochondria in the pathophysiology of this disorder. OXYS rats were treated with a mitochondria-targeted antioxidant SkQ1 from age 12 to 18 months, that is, during active progression of AD-like pathology in these animals. Dietary supplementation with SkQ1 caused this compound to accumulate in various brain regions, and it was localized mostly to neuronal mitochondria. Via improvement of structural and functional state of mitochondria, treatment with SkQ1 alleviated the structural neurodegenerative alterations, prevented the neuronal loss and synaptic damage, increased the levels of synaptic proteins, enhanced neurotrophic supply, and decreased amyloid-β1-42 protein levels and tau hyperphosphorylation in the hippocampus of OXYS rats, resulting in improvement of the learning ability and memory. Collectively, these data support that mitochondrial dysfunction may play a key role in the pathophysiology of AD and that therapies with target mitochondria are potent to normalize a wide range of cellular signaling processes and therefore slow the progression of AD.
                ER  -

Click to copy this citation from the text box above or download the citation:

Characterization of variations in IL23A and IL23R genes: possible roles in multiple sclerosis and other neuroinflammatory demyelinating diseases

Fei-Feng Li, Xi-Dong Zhu, Peng Yan, Mei-Hua Jin, Hui Yue, Qiong Zhang, Jin Fu, Shu-Lin Liu,

https://doi.org/10.18632/aging.101058 pp 2734—2746

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Li F, Zhu X, Yan P, Jin M, Yue H, Zhang Q, Fu J, Liu S, . Characterization of variations in IL23A and IL23R genes: possible roles in multiple sclerosis and other neuroinflammatory demyelinating diseases. . 8:2734-2746. https://doi.org/10.18632/aging.101058

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Li, Fei-Feng 
                AU  - Zhu, Xi-Dong 
                AU  - Yan, Peng 
                AU  - Jin, Mei-Hua 
                AU  - Yue, Hui 
                AU  - Zhang, Qiong 
                AU  - Fu, Jin 
                AU  - Liu, Shu-Lin 
                TI  - Characterization of variations in IL23A and IL23R genes: possible roles in multiple sclerosis and other neuroinflammatory demyelinating diseases
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101058
                DO  - 10.18632/aging.101058
                SP  - 2734
                EP  - 2746
                PY  - 
                AB  - Multiple sclerosis is among the most serious inflammatory demyelinating diseases (IDD). Interleukin-23A (IL23A) regulates and coordinates the activities of immune cells by interacting with its receptor IL23R and plays key roles in the pathogenesis of immune inflammatory diseases. IDD, deemed to be a kind of autoimmune diseases, may involve IL23A in the pathogenesis. The aim of this work was to validate the hypothesized involvement of IL-23A and its receptor in IDD. We sequenced the IL-23A and IL-23R genes for 206 Chinese Han IDD patients and evaluated SNPs within or near those genes. The serum levels of IL23A in IDD participants were analyzed using ELISA. The statistical analyses were conducted using Chi-Square Tests as implemented in SPSS (version 19.0). The Hardy-Weinberg equilibrium test of the population was carried out using online software OEGE. Three variants rs2066808, rs2371494, rs11575248 in IL-23A gene and one variant rs1884444 in IL-23R gene were demonstrated to be associated with the risk of MS or other IDD diseases, and the expression level of serum IL-23A in the MS patients was also altered. We conclude that variants in IL-23A and IL-23R genes were associated with the risk of MS or other IDD diseases.
                ER  -

Click to copy this citation from the text box above or download the citation:

PI3Kα inhibition reduces obesity in mice

Elena Lopez-Guadamillas, Maribel Muñoz-Martin, Sonia Martinez, Joaquin Pastor, Pablo J. Fernandez-Marcos, Manuel Serrano,

https://doi.org/10.18632/aging.101075 pp 2747—2753

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Lopez-Guadamillas E, Muñoz-Martin M, Martinez S, Pastor J, Fernandez-Marcos PJ, Serrano M, . PI3Kα inhibition reduces obesity in mice. . 8:2747-2753. https://doi.org/10.18632/aging.101075

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Lopez-Guadamillas, Elena 
                AU  - Muñoz-Martin, Maribel 
                AU  - Martinez, Sonia 
                AU  - Pastor, Joaquin 
                AU  - Fernandez-Marcos, Pablo J. 
                AU  - Serrano, Manuel 
                TI  - PI3Kα inhibition reduces obesity in mice
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101075
                DO  - 10.18632/aging.101075
                SP  - 2747
                EP  - 2753
                PY  - 
                AB  - Partial inhibition of PI3K is one of the best-validated and evolutionary conserved manipulations to extend longevity. The best known health beneficial effects of reduced PI3K are related to metabolism and include increased energy expenditure, reduced nutrient storage, and protection from obesity. We have previously shown that a dual chemical inhibitor of the alpha and delta PI3K isoforms (CNIO-PI3Ki) reduces obesity in mice and monkeys, without evident toxic effects after long-term treatment. Here, we dissect the role of the alpha and delta PI3K isoforms by making use of selective inhibitors against PI3Kα (BYL-719 also known as alpelisib) or PI3Kδ (GS-9820 also known as acalisib). Treatment of mice with the above mentioned inhibitors indicated that BYL-719 increases energy expenditure in normal mice and efficiently reduces body weight in obese (ob/ob) mice, whereas these effects were not observed with GS-9820. Of note, the dose of BYL-719 required to reduce obesity was 10x higher than the equivalent dose of CNIO-PI3Ki, which could suggest that simultaneous inhibition of PI3K alpha and delta is more beneficial than single inhibition of the alpha isoform. In summary, we conclude that inhibition of PI3Kα is sufficient to increase energy expenditure and reduce obesity, and suggest that concomitant PI3Kα inhibition could play an auxiliary role.
                ER  -

Click to copy this citation from the text box above or download the citation:

Aging is associated with an expansion of CD49f^hi mammary stem cells that show a decline in function and increased transformation potential

Qiaoxiang Dong, Hui Gao, Yuanshuo Shi, Fuchuang Zhang, Xiang Gu, Anqi Wu, Danhan Wang, Yuanhong Chen, Abhik Bandyopadhyay, I-Tien Yeh, Benjamin J. Daniel, Yidong Chen, Yi Zou, Vivienne L. Rebel, Christi A. Walter, Jianxin Lu, Changjiang Huang, Lu-Zhe Sun,

https://doi.org/10.18632/aging.101082 pp 2754—2776

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Dong Q, Gao H, Shi Y, Zhang F, Gu X, Wu A, Wang D, Chen Y, Bandyopadhyay A, Yeh I, Daniel BJ, Chen Y, Zou Y, et al, . Aging is associated with an expansion of CD49f^hi mammary stem cells that show a decline in function and increased transformation potential. . 8:2754-2776. https://doi.org/10.18632/aging.101082

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Dong, Qiaoxiang 
 AU - Gao, Hui 
 AU - Shi, Yuanshuo 
 AU - Zhang, Fuchuang 
 AU - Gu, Xiang 
 AU - Wu, Anqi 
 AU - Wang, Danhan 
 AU - Chen, Yuanhong 
 AU - Bandyopadhyay, Abhik 
 AU - Yeh, I-Tien 
 AU - Daniel, Benjamin J. 
 AU - Chen, Yidong 
 AU - Zou, Yi 
 AU - Rebel, Vivienne L. 
 AU - Walter, Christi A. 
 AU - Lu, Jianxin 
 AU - Huang, Changjiang 
 AU - Sun, Lu-Zhe 
 TI - Aging is associated with an expansion of CD49fhi mammary stem cells that show a decline in function and increased transformation potential
 JO - 
 JA - 
 VL - 8
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101082
 DO - 10.18632/aging.101082
 SP - 2754
 EP - 2776
 PY - 
 ER -

Provider: 
 TY - JOUR
 AU - Dong, Qiaoxiang 
 AU - Gao, Hui 
 AU - Shi, Yuanshuo 
 AU - Zhang, Fuchuang 
 AU - Gu, Xiang 
 AU - Wu, Anqi 
 AU - Wang, Danhan 
 AU - Chen, Yuanhong 
 AU - Bandyopadhyay, Abhik 
 AU - Yeh, I-Tien 
 AU - Daniel, Benjamin J. 
 AU - Chen, Yidong 
 AU - Zou, Yi 
 AU - Rebel, Vivienne L. 
 AU - Walter, Christi A. 
 AU - Lu, Jianxin 
 AU - Huang, Changjiang 
 AU - Sun, Lu-Zhe 
 TI - Aging is associated with an expansion of CD49fhi mammary stem cells that show a decline in function and increased transformation potential
 JO - 
 JA - 
 VL - 8
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101082
 DO - 10.18632/aging.101082
 SP - 2754
 EP - 2776
 PY - 
 AB - Breast cancer incidence increases during aging, yet the mechanism of age-associated mammary tumorigenesis is unclear. Mammary stem cells are believed to play an important role in breast tumorigenesis, but how their function changes with age is unknown. We compared mammary epithelial cells isolated from young and old mammary glands of different cohorts of C57BL6/J and BALB/c mice, and our findings revealed that old mammary glands were characterized by increased basal cell pool comprised of mostly CD49fhi cells, altered luminal-to-basal cell ratio, and irregular ductal morphology. More interestingly, basal stem cells in old mice were increased in frequency, but showed a functional decline of differentiation and increased neoplastic transformation potential. Gene signature enrichment analysis revealed a significant enrichment of a luminal cell gene expression signature in the basal stem cell-enriched population from old mice, suggesting some luminal cells were expressing basal markers. Immunofluorescence staining confirmed the presence of luminal cells with high CD49f expression in hyperplastic lesions implicating these cells as undergoing luminal to basal phenotypic changes during aging. Whole transcriptome analysis showed elevated immune and inflammatory responses in old basal stem cells and stromal cells, which may be the underlying cause for increased CD49fhi basal-like cells in aged glands.
 ER -

Click to copy this citation from the text box above or download the citation:

Long-term caloric restriction in ApoE-deficient mice results in neuroprotection via Fgf21-induced AMPK/mTOR pathway

Claire Rühlmann, Tjark Wölk, Tobias Blümel, Laura Stahn, Brigitte Vollmar, Angela Kuhla,

https://doi.org/10.18632/aging.101086 pp 2777—2789

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Rühlmann C, Wölk T, Blümel T, Stahn L, Vollmar B, Kuhla A, . Long-term caloric restriction in ApoE-deficient mice results in neuroprotection via Fgf21-induced AMPK/mTOR pathway. . 8:2777-2789. https://doi.org/10.18632/aging.101086

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Rühlmann, Claire 
 AU - Wölk, Tjark 
 AU - Blümel, Tobias 
 AU - Stahn, Laura 
 AU - Vollmar, Brigitte 
 AU - Kuhla, Angela 
 TI - Long-term caloric restriction in ApoE-deficient mice results in neuroprotection via Fgf21-induced AMPK/mTOR pathway
 JO - 
 JA - 
 VL - 8
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101086
 DO - 10.18632/aging.101086
 SP - 2777
 EP - 2789
 PY - 
 AB - Caloric restriction (CR) decelerates the aging process, extends lifespan and exerts neuroprotective effects in diverse species by so far unknown mechanisms. Based on known neuroprotective effects of fibroblastic growth factor 21 (Fgf21) we speculate that CR upregulates Fgf21, which phosphorylates neuronal AMP-activated protein kinase (AMPK), leading to a decrease of mammalian target of rapamycin (mTOR) signaling activity and an inhibition of tau-hyperphosphorylation. This in turn reduces the formation of neurofibrillary tangles, a neuropathological hallmark of Alzheimer´s disease. ApoE-deficient mice (ApoE-/-), serving as a model of neurodegeneration, showed upon CR vs. ad libitum feeding increased Fgf21 levels in both, plasma and brain as well as higher phosphorylation of fibroblastic growth factor receptor 1c (Fgfr1c), extracellular signal-regulated kinases 1/2 (ERK1/2) and AMPK in brain, lower activity of mTOR and decreased Tau-phosphorylation. Finally, CR in ApoE-/- mice caused neuroprotection as indicated by a higher synaptic plasticity shown by immunohistochemical analysis with increased numbers of PSD95-positive neurons and a better cognitive performance as analyzed with Morris water maze test. These data provide substantial evidence that neuroprotection upon CR seems to be Fgf21-dependent. Further experiments are necessary to evaluate Fgf21 as a therapeutic tool to treat tauopathy for improvement of cognitive performance.
 ER -

Click to copy this citation from the text box above or download the citation:

Expression of Rab1A is upregulated in human lung cancer and associated with tumor size and T stage

Xinxin Wang, Feng Liu, Xiaoyu Qin, Tinglei Huang, Bo Huang, Yanjie Zhang, Bin Jiang,

https://doi.org/10.18632/aging.101087 pp 2790—2798

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wang X, Liu F, Qin X, Huang T, Huang B, Zhang Y, Jiang B, . Expression of Rab1A is upregulated in human lung cancer and associated with tumor size and T stage. . 8:2790-2798. https://doi.org/10.18632/aging.101087

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wang, Xinxin 
                AU  - Liu, Feng 
                AU  - Qin, Xiaoyu 
                AU  - Huang, Tinglei 
                AU  - Huang, Bo 
                AU  - Zhang, Yanjie 
                AU  - Jiang, Bin 
                TI  - Expression of Rab1A is upregulated in human lung cancer and associated with tumor size and T stage
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101087
                DO  - 10.18632/aging.101087
                SP  - 2790
                EP  - 2798
                PY  - 
                AB  - Rab1A expression is associated with malignant phenotypes in several human tumors; however, the role of Rab1A in lung cancer is still unclear. In this study, we attempted to establish the role of Rab1A in major human lung cancer subtypes. Rab1A expression in different histological types of human lung cancer was analyzed in lung cancer tissues with paired adjacent noncancerous tissues and a large panel of lung cancer cell lines. The effect of Rab1A expression on multiple cancer-associated signaling pathways was also examined. The results demonstrated that Rab1A was significantly overexpressed in the different histological types of lung cancer as compared to non-cancerous tissues, and Rab1A expression was correlated with tumor volume and stage. In a large panel of lung cancer cell lines, high Rab1A expression was observed as compared to a normal lung/bronchus epithelial cell line. However, Rab1A protein levels were not correlated with mTORC1 (P-S6K1), mTORC2 (P-AKT), MEK (P-ERK), JNK (P-c-Jun) or p38MAPK (P-MK2) signaling. Rab1A knockdown had no effect on mTOR signaling or cell growth. These data suggested that Rab1A may be involved in the pathogenesis of human lung cancer in an mTOR- and MAPK-independent manner.
                ER  -

Click to copy this citation from the text box above or download the citation:

Expansion induced microRNA changes in bone marrow mesenchymal stromal cells reveals interplay between immune regulation and cell cycle

Lotta Kilpinen, Amarjit Parmar, Dario Greco, Matti Korhonen, Petri Lehenkari, Päivi Saavalainen, Saara Laitinen,

https://doi.org/10.18632/aging.101088 pp 2799—2813

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Kilpinen L, Parmar A, Greco D, Korhonen M, Lehenkari P, Saavalainen P, Laitinen S, . Expansion induced microRNA changes in bone marrow mesenchymal stromal cells reveals interplay between immune regulation and cell cycle. . 8:2799-2813. https://doi.org/10.18632/aging.101088

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Kilpinen, Lotta 
                AU  - Parmar, Amarjit 
                AU  - Greco, Dario 
                AU  - Korhonen, Matti 
                AU  - Lehenkari, Petri 
                AU  - Saavalainen, Päivi 
                AU  - Laitinen, Saara 
                TI  - Expansion induced microRNA changes in bone marrow mesenchymal stromal cells reveals interplay between immune regulation and cell cycle
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101088
                DO  - 10.18632/aging.101088
                SP  - 2799
                EP  - 2813
                PY  - 
                AB  - Mesenchymal stromal cells (MSC) are currently used in many cell based therapies. Prior to use in therapy, extensive expansion is required. We used microarray profiling to investigate expansion induced miRNA and mRNA expression changes of bone marrow MSCs (BM-MSCs) derived from old and young donors. The expression levels of 36 miRNAs were altered in cells derived from the old and respectively 39 miRNAs were altered in cells derived from young donors. Of these, only 12 were differentially expressed in both young and old donor BM-MSCs, and their predicted target mRNAs, were mainly linked to cell proliferation and senescence. Further qPCR verification showed that the expression of miR-1915-3p, miR-1207, miR-3665, and miR-762 correlated with the expansion time at passage 8. Previously described BM-MSC-specific miRNA fingerprints were also detected but these remained unchanged during expansion. Interestingly, members of well-studied miR-17/92 cluster, involved in cell cycle regulation, aging and also development of immune system, were down-regulated specifically in cells from old donors. The role of this cluster in MSC functionality is worth future studies since it links expansion, aging and immune system together.
                ER  -

Click to copy this citation from the text box above or download the citation:

Caloric restriction preserves memory and reduces anxiety of aging mice with early enhancement of neurovascular functions

Ishita Parikh, Janet Guo, Kai-Hsiang Chuang, Yu Zhong, Ralf G. Rempe, Jared D. Hoffman, Rachel Armstrong, Björn Bauer, Anika M.S. Hartz, Ai-Ling Lin,

https://doi.org/10.18632/aging.101094 pp 2814—2826

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Parikh I, Guo J, Chuang K, Zhong Y, Rempe RG, Hoffman JD, Armstrong R, Bauer B, Hartz AM, Lin A, . Caloric restriction preserves memory and reduces anxiety of aging mice with early enhancement of neurovascular functions. . 8:2814-2826. https://doi.org/10.18632/aging.101094

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Parikh, Ishita 
                AU  - Guo, Janet 
                AU  - Chuang, Kai-Hsiang 
                AU  - Zhong, Yu 
                AU  - Rempe, Ralf G. 
                AU  - Hoffman, Jared D. 
                AU  - Armstrong, Rachel 
                AU  - Bauer, Björn 
                AU  - Hartz, Anika M.S. 
                AU  - Lin, Ai-Ling 
                TI  - Caloric restriction preserves memory and reduces anxiety of aging mice with early enhancement of neurovascular functions
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101094
                DO  - 10.18632/aging.101094
                SP  - 2814
                EP  - 2826
                PY  - 
                AB  - Neurovascular integrity plays an important role in protecting cognitive and mental health in aging. Lifestyle interventions that sustain neurovascular integrity may thus be critical on preserving brain functions in aging and reducing the risk for age-related neurodegenerative disorders. Here we show that caloric restriction (CR) had an early effect on neurovascular enhancements, and played a critical role in preserving vascular, cognitive and mental health in aging. In particular, we found that CR significantly enhanced cerebral blood flow (CBF) and blood-brain barrier function in young mice at 5-6 months of age. The neurovascular enhancements were associated with reduced mammalian target of rapamycin expression, elevated endothelial nitric oxide synthase signaling, and increased ketone bodies utilization. With age, CR decelerated the rate of decline in CBF. The preserved CBF in hippocampus and frontal cortex were highly correlated with preserved memory and learning, and reduced anxiety, of the aging mice treated with CR (18-20 months of age). Our results suggest that dietary intervention started in the early stage (e.g., young adults) may benefit cognitive and mental reserve in aging. Understanding nutritional effects on neurovascular functions may have profound implications in human brain aging and age-related neurodegenerative disorders.
                ER  -

Click to copy this citation from the text box above or download the citation:

Tethering telomerase to telomeres increases genome instability and promotes chronological aging in yeast

Jun Liu, Ming-Hong He, Jing Peng, Yi-Min Duan, Yi-Si Lu, Zhenfang Wu, Ting Gong, Hong-Tao Li, Jin-Qiu Zhou,

https://doi.org/10.18632/aging.101095 pp 2827—2847

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Liu J, He M, Peng J, Duan Y, Lu Y, Wu Z, Gong T, Li H, Zhou J, . Tethering telomerase to telomeres increases genome instability and promotes chronological aging in yeast. . 8:2827-2847. https://doi.org/10.18632/aging.101095

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Liu, Jun 
                AU  - He, Ming-Hong 
                AU  - Peng, Jing 
                AU  - Duan, Yi-Min 
                AU  - Lu, Yi-Si 
                AU  - Wu, Zhenfang 
                AU  - Gong, Ting 
                AU  - Li, Hong-Tao 
                AU  - Zhou, Jin-Qiu 
                TI  - Tethering telomerase to telomeres increases genome instability and promotes chronological aging in yeast
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101095
                DO  - 10.18632/aging.101095
                SP  - 2827
                EP  - 2847
                PY  - 
                AB  - Chronological aging of the yeast Saccharomyces cerevisiae is attributed to multi-faceted traits especially those involving genome instability, and has been considered to be an aging model for post-mitotic cells in higher organisms. Telomeres are the physical ends of eukaryotic chromosomes, and are essential for genome integrity and stability. It remains elusive whether dysregulated telomerase activity affects chronological aging. We employed the CDC13-EST2 fusion gene, which tethers telomerase to telomeres, to examine the effect of constitutively active telomerase on chronological lifespan (CLS). The expression of Cdc13-Est2 fusion protein resulted in overlong telomeres (2 to 4 folds longer than normal telomeres), and long telomeres were stably maintained during long-term chronological aging. Accordingly, genome instability, manifested by accumulation of extra-chromosomal rDNA circle species, age-dependent CAN1 marker-gene mutation frequency and gross chromosomal rearrangement frequency, was significantly elevated. Importantly, inactivation of Sch9, a downstream kinase of the target of rapamycin complex 1 (TORC1), suppressed both the genome instability and accelerated chronological aging mediated by CDC13-EST2 expression. Interestingly, loss of the CDC13-EST2 fusion gene in the cells with overlong telomeres restored the regular CLS. Altogether, these data suggest that constitutively active telomerase is detrimental to the maintenance of genome stability, and promotes chronological aging in yeast.
                ER  -

Click to copy this citation from the text box above or download the citation:

No effect of testosterone on behavior in aged Wistar rats

Veronika Borbélyová, Emese Domonkos, Janka Bábíčková, Ľubomíra Tóthová, Martin Bosý, Július Hodosy, Peter Celec,

https://doi.org/10.18632/aging.101096 pp 2848—2861

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Borbélyová V, Domonkos E, Bábíčková J, Tóthová Ľ, Bosý M, Hodosy J, Celec P, . No effect of testosterone on behavior in aged Wistar rats. . 8:2848-2861. https://doi.org/10.18632/aging.101096

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Borbélyová, Veronika 
                AU  - Domonkos, Emese 
                AU  - Bábíčková, Janka 
                AU  - Tóthová, Ľubomíra 
                AU  - Bosý, Martin 
                AU  - Hodosy, Július 
                AU  - Celec, Peter 
                TI  - No effect of testosterone on behavior in aged Wistar rats
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101096
                DO  - 10.18632/aging.101096
                SP  - 2848
                EP  - 2861
                PY  - 
                AB  - In men, aging is accompanied by a gradual decline in androgen secretion. Studies suggest beneficial effects of endogenous and exogenous testosterone on affective behavior and cognitive functions. The aim of this study was to describe behavioral and cognitive sex differences and to analyze the effects of long-term androgen deficiency in aged male rats. Thirty-months old rats divided into three groups (males, females and males gonadectomized as young adults) underwent a battery of behavioral tests assessing locomotor activity, anxiety, memory, anhedonia, sociability and depression-like behavior. No major effect of gonadectomy was found in any of the analyzed behavioral measures in male rats. The only consistent sex difference was confirmed in depression-like behavior with longer immobility time observed in males. In an interventional experiment, a single dose of testosterone had no effect on gonadectomized male and female rats in the forced swim test. In contrast to previous studies this comprehensive behavioral phenotyping of aged rats revealed no major role of endogenous testosterone. Based on our results long-term hypogonadism does not alter the behavior of aged male rats, neither does acute testosterone treatment. Whether these findings have any consequences on androgen replacement therapy in aged men remains to be elucidated.
                ER  -

Click to copy this citation from the text box above or download the citation:

Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naïve patients

Chenghao Su, Yong Lin, Qianguo Mao, Daitze Wu, Lina Zhu, Isabel Najera, Fernando Garcia-Alcalde, Jianjun Niu,

https://doi.org/10.18632/aging.101097 pp 2862—2870

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Su C, Lin Y, Mao Q, Wu D, Zhu L, Najera I, Garcia-Alcalde F, Niu J, . Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naïve patients. . 8:2862-2870. https://doi.org/10.18632/aging.101097

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Su, Chenghao 
                AU  - Lin, Yong 
                AU  - Mao, Qianguo 
                AU  - Wu, Daitze 
                AU  - Zhu, Lina 
                AU  - Najera, Isabel 
                AU  - Garcia-Alcalde, Fernando 
                AU  - Niu, Jianjun 
                TI  - Association study between mannose-binding lectin haplotypes and X gene mutation of hepatitis B virus from treatment naïve patients
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101097
                DO  - 10.18632/aging.101097
                SP  - 2862
                EP  - 2870
                PY  - 
                AB  - Mannose binding lectin (MBL) plays important role in the innate immunity of human. Mutations in the MBL2 gene can significantly change the serum level of MBL, and consequently alter the susceptibility and progression of infectious disease. However, the association between the MBL2 profile and the HBV mutation and quasispecies complexity has not yet been reported. Our approach includes the study of the MBL2 gene genotype as well as ultra-deep sequencing of the HBV viruses obtained from the plasma of 50 treatment naïve patients with chronic HBV infection. We found that the liver function was better among patients within the high MBL2 group with respect to those within the medium/low MBL2 group. Likewise, the number of mutations in the HBV X gene as well as the viral quasispecies complexity were significantly higher in medium/low MBL2 production group. Nucleotide substitution rates were also higher within the medium/low MBL2 production group in all positions described to have an influence in liver cancer development, except for A1499G. In this work we show that the MBL2 profile may have an impact on the HBV X gene mutations as well as on viral quasispecies complexity.
                ER  -

Click to copy this citation from the text box above or download the citation:

Age-associated NF-κB signaling in myofibers alters the satellite cell niche and re-strains muscle stem cell function

Juhyun Oh, Indranil Sinha, Kah Yong Tan, Bernard Rosner, Jonathan M. Dreyfuss, Ornela Gjata, Peter Tran, Steven E. Shoelson, Amy J. Wagers,

https://doi.org/10.18632/aging.101098 pp 2871—2896

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Oh J, Sinha I, Tan KY, Rosner B, Dreyfuss JM, Gjata O, Tran P, Shoelson SE, Wagers AJ, . Age-associated NF-κB signaling in myofibers alters the satellite cell niche and re-strains muscle stem cell function. . 8:2871-2896. https://doi.org/10.18632/aging.101098

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Oh, Juhyun 
                AU  - Sinha, Indranil 
                AU  - Tan, Kah Yong 
                AU  - Rosner, Bernard 
                AU  - Dreyfuss, Jonathan M. 
                AU  - Gjata, Ornela 
                AU  - Tran, Peter 
                AU  - Shoelson, Steven E. 
                AU  - Wagers, Amy J. 
                TI  - Age-associated NF-κB signaling in myofibers alters the satellite cell niche and re-strains muscle stem cell function
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101098
                DO  - 10.18632/aging.101098
                SP  - 2871
                EP  - 2896
                PY  - 
                AB  - Skeletal muscle is a highly regenerative tissue, but muscle repair potential is increasingly compromised with advancing age. In this study, we demonstrate that increased NF-κB activity in aged muscle fibers contributes to diminished myogenic potential of their associated satellite cells. We further examine the impact of genetic modulation of NF-κB signaling in muscle satellite cells or myofibers on recovery after damage. These studies reveal that NF-κB activity in differentiated myofibers is sufficient to drive dysfunction of muscle regenerative cells via cell-non-autonomous mechanisms. Inhibition of NF-κB, or its downstream target Phospholipase A2, in myofibers rescued muscle regenerative potential in aged muscle. Moreover, systemic administration of sodium salicylate, an FDA-approved NF-κB inhibitor, decreased inflammatory gene expression and improved repair in aged muscle. Together, these studies identify a unique NF-κB regulated, non-cell autonomous mechanism by which stem cell function is linked to lipid signaling and homeostasis, and provide important new targets to stimulate muscle repair in aged individuals.
                ER  -

Click to copy this citation from the text box above or download the citation:

Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice

Rachel A. Gioscia-Ryan, Micah L. Battson, Lauren M. Cuevas, Melanie C. Zigler, Amy L. Sindler, Douglas R. Seals,

https://doi.org/10.18632/aging.101099 pp 2897—2914

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Gioscia-Ryan RA, Battson ML, Cuevas LM, Zigler MC, Sindler AL, Seals DR, . Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice. . 8:2897-2914. https://doi.org/10.18632/aging.101099

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Gioscia-Ryan, Rachel A. 
                AU  - Battson, Micah L. 
                AU  - Cuevas, Lauren M. 
                AU  - Zigler, Melanie C. 
                AU  - Sindler, Amy L. 
                AU  - Seals, Douglas R. 
                TI  - Voluntary aerobic exercise increases arterial resilience and mitochondrial health with aging in mice
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101099
                DO  - 10.18632/aging.101099
                SP  - 2897
                EP  - 2914
                PY  - 
                AB  - Mitochondrial dysregulation and associated excessive reactive oxygen species (mtROS) production is a key source of oxidative stress in aging arteries that reduces baseline function and may influence resilience (ability to withstand stress). We hypothesized that voluntary aerobic exercise would increase arterial resilience in old mice. An acute mitochondrial stressor (rotenone) caused greater (further) impairment in peak carotid EDD in old (~27 mo., OC, n=12; -32.5±-10.5%) versus young (~7 mo., YC n=11; -5.4±- 3.7%) control male mice, whereas arteries from young and old exercising (YVR n=10 and OVR n=11, 10-wk voluntary running; -0.8±-2.1% and -8.0±4.9%, respectively) mice were protected. Ex-vivo simulated Western diet (WD, high glucose and palmitate) caused greater impairment in EDD in OC (-28.5±8.6%) versus YC (-16.9±5.2%) and YVR (-15.3±2.3%), whereas OVR (-8.9±3.9%) were more resilient (not different versus YC). Simultaneous ex-vivo treatment with mitochondria-specific antioxidant MitoQ attenuated WD-induced impairments in YC and OC, but not YVR or OVR, suggesting that exercise improved resilience to mtROS-mediated stress. Exercise normalized age-related alterations in aortic mitochondrial protein markers PGC-1α, SIRT-3 and Fis1 and augmented cellular antioxidant and stress response proteins. Our results indicate that arterial aging is accompanied by reduced resilience and mitochondrial health, which are restored by voluntary aerobic exercise.
                ER  -

Click to copy this citation from the text box above or download the citation:

Discovery of piperlongumine as a potential novel lead for the development of senolytic agents

Yingying Wang, Jianhui Chang, Xingui Liu, Xuan Zhang, Suping Zhang, Xin Zhang, Daohong Zhou, Guangrong Zheng,

https://doi.org/10.18632/aging.101100 pp 2915—2926

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Wang Y, Chang J, Liu X, Zhang X, Zhang S, Zhang X, Zhou D, Zheng G, . Discovery of piperlongumine as a potential novel lead for the development of senolytic agents. . 8:2915-2926. https://doi.org/10.18632/aging.101100

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Wang, Yingying 
                AU  - Chang, Jianhui 
                AU  - Liu, Xingui 
                AU  - Zhang, Xuan 
                AU  - Zhang, Suping 
                AU  - Zhang, Xin 
                AU  - Zhou, Daohong 
                AU  - Zheng, Guangrong 
                TI  - Discovery of piperlongumine as a potential novel lead for the development of senolytic agents
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101100
                DO  - 10.18632/aging.101100
                SP  - 2915
                EP  - 2926
                PY  - 
                AB  - Accumulating evidence indicates that senescent cells play an important role in many age-associated diseases. The pharmacological depletion of senescent cells (SCs) with a “senolytic agent”, a small molecule that selectively kills SCs, is a potential novel therapeutic approach for these diseases. Recently, we discovered ABT-263, a potent and highly selective senolytic agent, by screening a library of rationally-selected compounds. With this screening approach, we also identified a second senolytic agent called piperlongumine (PL). PL is a natural product that is reported to have many pharmacological effects, including anti-tumor activity. We show here that PL preferentially killed senescent human WI-38 fibroblasts when senescence was induced by ionizing radiation, replicative exhaustion, or ectopic expression of the oncogene Ras. PL killed SCs by inducing apoptosis, and this process did not require the induction of reactive oxygen species. In addition, we found that PL synergistically killed SCs in combination with ABT-263, and initial structural modifications to PL identified analogs with improved potency and/or selectivity in inducing SC death. Overall, our studies demonstrate that PL is a novel lead for developing senolytic agents.
                ER  -

Click to copy this citation from the text box above or download the citation:

Regulation of human cerebrospinal fluid malate dehydrogenase 1 in sporadic Creutzfeldt-Jakob disease patients

Matthias Schmitz, Franc Llorens, Alexander Pracht, Tobias Thom, Ângela Correia, Saima Zafar, Isidre Ferrer, Inga Zerr,

https://doi.org/10.18632/aging.101101 pp 2927—2935

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Schmitz M, Llorens F, Pracht A, Thom T, Correia Â, Zafar S, Ferrer I, Zerr I, . Regulation of human cerebrospinal fluid malate dehydrogenase 1 in sporadic Creutzfeldt-Jakob disease patients. . 8:2927-2935. https://doi.org/10.18632/aging.101101

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Schmitz, Matthias 
                AU  - Llorens, Franc 
                AU  - Pracht, Alexander 
                AU  - Thom, Tobias 
                AU  - Correia, Ângela 
                AU  - Zafar, Saima 
                AU  - Ferrer, Isidre 
                AU  - Zerr, Inga 
                TI  - Regulation of human cerebrospinal fluid malate dehydrogenase 1 in sporadic Creutzfeldt-Jakob disease patients
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101101
                DO  - 10.18632/aging.101101
                SP  - 2927
                EP  - 2935
                PY  - 
                AB  - The identification of reliable diagnostic biomarkers in differential diagnosis of neurodegenerative diseases is an ongoing topic. A previous two-dimensional proteomic study on cerebrospinal fluid (CSF) revealed an elevated level of an enzyme, mitochondrial malate dehydrogenase 1 (MDH1), in sporadic Creutzfeldt-Jakob disease (sCJD) patients. Here, we could demonstrate the expression of MDH1 in neurons as well as in the neuropil. Its levels are lower in sCJD brains than in control brains. An examination of CSF-MDH1 in sCJD patients by ELISA revealed a significant elevation of CSF-MDH1 levels in sCJD patients (independently from the PRNP codon 129 MV genotype or the prion protein scrapie (PrPSc) type) in comparison to controls. In combination with total tau (tau), CSF-MDH1 detection exhibited a high diagnostic accuracy for sCJD diagnosis with a sensitivity of 97.5% and a specificity of 95.6%. A correlation study of MDH1 level in CSF with other neurodegenerative marker proteins revealed a significant positive correlation between MDH1 concentration with tau, 14-3-3 and neuron specific enolase level. In conclusion, our study indicated the potential of MDH1 in combination with tau as an additional biomarker in sCJD improving diagnostic accuracy of tau markedly.
                ER  -

Click to copy this citation from the text box above or download the citation:

Molecular pathway activation features of pediatric acute myeloid leukemia (AML) and acute lymphoblast leukemia (ALL) cells

Ivan Petrov, Maria Suntsova, Olga Mutorova, Maxim Sorokin, Andrew Garazha, Elena Ilnitskaya, Pavel Spirin, Sergey Larin, Olga Kovalchuk, Vladimir Prassolov, Alex Zhavoronkov, Alexander Roumiantsev, Anton Buzdin,

https://doi.org/10.18632/aging.101102 pp 2936—2947

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Petrov I, Suntsova M, Mutorova O, Sorokin M, Garazha A, Ilnitskaya E, Spirin P, Larin S, Kovalchuk O, Prassolov V, Zhavoronkov A, Roumiantsev A, Buzdin A, . Molecular pathway activation features of pediatric acute myeloid leukemia (AML) and acute lymphoblast leukemia (ALL) cells. . 8:2936-2947. https://doi.org/10.18632/aging.101102

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Petrov, Ivan 
                AU  - Suntsova, Maria 
                AU  - Mutorova, Olga 
                AU  - Sorokin, Maxim 
                AU  - Garazha, Andrew 
                AU  - Ilnitskaya, Elena 
                AU  - Spirin, Pavel 
                AU  - Larin, Sergey 
                AU  - Kovalchuk, Olga 
                AU  - Prassolov, Vladimir 
                AU  - Zhavoronkov, Alex 
                AU  - Roumiantsev, Alexander 
                AU  - Buzdin, Anton 
                TI  - Molecular pathway activation features of pediatric acute myeloid leukemia (AML) and acute lymphoblast leukemia (ALL) cells
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101102
                DO  - 10.18632/aging.101102
                SP  - 2936
                EP  - 2947
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Petrov, Ivan 
                AU  - Suntsova, Maria 
                AU  - Mutorova, Olga 
                AU  - Sorokin, Maxim 
                AU  - Garazha, Andrew 
                AU  - Ilnitskaya, Elena 
                AU  - Spirin, Pavel 
                AU  - Larin, Sergey 
                AU  - Kovalchuk, Olga 
                AU  - Prassolov, Vladimir 
                AU  - Zhavoronkov, Alex 
                AU  - Roumiantsev, Alexander 
                AU  - Buzdin, Anton 
                TI  - Molecular pathway activation features of pediatric acute myeloid leukemia (AML) and acute lymphoblast leukemia (ALL) cells
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101102
                DO  - 10.18632/aging.101102
                SP  - 2936
                EP  - 2947
                PY  - 
                AB  - Acute lymphoblast leukemia (ALL) is characterized by overproduction of immature white blood cells in the bone marrow. ALL is most common in the childhood and has high (&gt;80%) cure rate. In contrast, acute myeloid leukemia (AML) has far greater mortality rate than the ALL and is most commonly affecting older adults. However, AML is a leading cause of childhood cancer mortality. In this study, we compare gene expression and molecular pathway activation patterns in three normal blood, seven pediatric ALL and seven pediatric AML bone marrow samples. We identified 172/94 and 148/31 characteristic gene expression/pathway activation signatures, clearly distinguishing pediatric ALL and AML cells, respectively, from the normal blood. The pediatric AML and ALL cells differed by 139/34 gene expression/pathway activation biomarkers. For the adult 30 AML and 17 normal blood samples, we found 132/33 gene expression/pathway AML-specific features, of which only 7/2 were common for the adult and pediatric AML and, therefore, age-independent. At the pathway level, we found more differences than similarities between the adult and pediatric forms. These findings suggest that the adult and pediatric AMLs may require different treatment strategies.
                ER  -

Click to copy this citation from the text box above or download the citation:

Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p

Peng Song, Shu-Cheng Yin,

https://doi.org/10.18632/aging.101103 pp 2948—2960

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Song P, Yin S, . Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p. . 8:2948-2960. https://doi.org/10.18632/aging.101103

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Song, Peng 
                AU  - Yin, Shu-Cheng 
                TI  - Long non-coding RNA EWSAT1 promotes human nasopharyngeal carcinoma cell growth in vitro by targeting miR-326/-330-5p
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101103
                DO  - 10.18632/aging.101103
                SP  - 2948
                EP  - 2960
                PY  - 
                AB  - Long non-coding RNA (lncRNA) Ewing sarcoma associated transcript 1 (EWSAT1) has been identified as an oncogene, and its dysregulation is closed corrected with tumor progression in Ewing sarcoma. Recently, high-through put analysis reveals that EWSAT1 is also highly expressed in human nasopharyngeal carcinoma (NPC). However, whether the aberrant expression of EWSAT1 in NPC is corrected with malignancy or prognosis has not been expounded. Herein, we identified that EWSAT1 was up-regulated in NPC tissues and cell lines, and higher expression of EWSAT1 resulted in a markedly poorer survival time. EWSAT1 over-expression facilitated, while EWSAT1 silencing impaired cell growth in NPC. In addition, mechanistic analysis demonstrated that EWSAT1 up-regulated the expression of miR-326/330-5p clusters targeted gene cyclin D1 through acting as a competitive ‘sponge’ of miR-326/330-5p clusters. Collectively, our data revealed that EWSAT1 promotes NPC cell growth in vitro through up-regulating cyclin D1 partially via ‘spongeing’ miR-326/330-5p clusters.
                ER  -

Click to copy this citation from the text box above or download the citation:

Depressive symptoms are associated with leukocyte telomere length in American Indians: findings from the Strong Heart Family Study

Qi Zhao, Yun Zhu, Fawn Yeh, Jue Lin, Elisa T. Lee, Shelley A. Cole, Darren Calhoun, Jinying Zhao,

https://doi.org/10.18632/aging.101104 pp 2961—2970

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Zhao Q, Zhu Y, Yeh F, Lin J, Lee ET, Cole SA, Calhoun D, Zhao J, . Depressive symptoms are associated with leukocyte telomere length in American Indians: findings from the Strong Heart Family Study. . 8:2961-2970. https://doi.org/10.18632/aging.101104

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Zhao, Qi 
                AU  - Zhu, Yun 
                AU  - Yeh, Fawn 
                AU  - Lin, Jue 
                AU  - Lee, Elisa T. 
                AU  - Cole, Shelley A. 
                AU  - Calhoun, Darren 
                AU  - Zhao, Jinying 
                TI  - Depressive symptoms are associated with leukocyte telomere length in American Indians: findings from the Strong Heart Family Study
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101104
                DO  - 10.18632/aging.101104
                SP  - 2961
                EP  - 2970
                PY  - 
                AB  - Patients with depression have an increased risk for many aging-related disorders, but the biological mechanisms underlying this link remain to be determined. Here we examined the association between depressive symptoms and leukocyte telomere length (LTL), a marker of biological aging, among 2,175 American Indians participating in the Strong Heart Family Study. Depressive symptoms were assessed by the Center for Epidemiologic Studies of Depression Scale (CES-D), which was categorized into four levels: none (&lt; 10), mild (10-15), moderate (16 -24), and severe (&gt; 24). LTL (T/S ratio) was quantified by qPCR. The association between depressive symptoms and LTL was examined by multivariate generalized estimating equation models, adjusting for sociodemographic factors, lifestyle factors, and chronic conditions. Results showed that individuals with a higher level of depressive symptoms had shorter LTL. Specifically, LTL in participants reporting none, mild, moderate, and severe depressive symptoms were 1.000, 0.999, 0.988, and 0.966, respectively (P for trend = 0.0278). Moreover, gender appears to modulate the effect of reported depressive symptoms that fall in the severe range (CES-D &gt; 24) on LTL (P for interaction = 0.0346). Our results suggest that depressive symptoms may accelerate biological aging through pathways beyond traditional risk factors in American Indians.
                ER  -

Click to copy this citation from the text box above or download the citation:

A serum miRNA profile of human longevity: findings from the Baltimore Longitudinal Study of Aging (BLSA)

Thalyana Smith-Vikos, Zuyun Liu, Christine Parsons, Myriam Gorospe, Luigi Ferrucci, Thomas M. Gill, Frank J. Slack,

https://doi.org/10.18632/aging.101106 pp 2971—2987

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Smith-Vikos T, Liu Z, Parsons C, Gorospe M, Ferrucci L, Gill TM, Slack FJ, . A serum miRNA profile of human longevity: findings from the Baltimore Longitudinal Study of Aging (BLSA). . 8:2971-2987. https://doi.org/10.18632/aging.101106

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Smith-Vikos, Thalyana 
                AU  - Liu, Zuyun 
                AU  - Parsons, Christine 
                AU  - Gorospe, Myriam 
                AU  - Ferrucci, Luigi 
                AU  - Gill, Thomas M. 
                AU  - Slack, Frank J. 
                TI  - A serum miRNA profile of human longevity: findings from the Baltimore Longitudinal Study of Aging (BLSA)
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101106
                DO  - 10.18632/aging.101106
                SP  - 2971
                EP  - 2987
                PY  - 
                AB  - In C. elegans, miRNAs are genetic biomarkers of aging. Similarly, multiple miRNAs are differentially expressed between younger and older persons, suggesting that miRNA-regulated biological mechanisms affecting aging are evolutionarily conserved. Previous human studies have not considered participants’ lifespans, a key factor in identifying biomarkers of aging. Using PCR arrays, we measured miRNA levels from serum samples obtained longitudinally at ages 50, 55, and 60 from 16 non-Hispanic males who had documented lifespans from 58 to 92. Numerous miRNAs showed significant changes in expression levels. At age 50, 24 miRNAs were significantly upregulated, and 73 were significantly downregulated in the long-lived subgroup (76-92 years) as compared with the short-lived subgroup (58-75 years). In long-lived participants, the most upregulated was miR-373-5p, while the most downregulated was miR-15b-5p. Longitudinally, significant Pearson correlations were observed between lifespan and expression of nine miRNAs (p value&lt;0.05). Six of these nine miRNAs (miR-211-5p, 374a-5p, 340-3p, 376c-3p, 5095, 1225-3p) were also significantly up- or downregulated when comparing long-lived and short-lived participants. Twenty-four validated targets of these miRNAs encoded aging-associated proteins, including PARP1, IGF1R, and IGF2R. We propose that the expression profiles of the six miRNAs (miR-211-5p, 374a-5p, 340-3p, 376c-3p, 5095, and 1225-3p) may be useful biomarkers of aging.
                ER  -

Click to copy this citation from the text box above or download the citation:

Transgenerational programming of longevity through E(z)-mediated histone H3K27 trimethylation in Drosophila

Brian Xia, Ed Gerstin, Dustin E. Schones, Wendong Huang, J. Steven de Belle,

https://doi.org/10.18632/aging.101107 pp 2988—3008

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Xia B, Gerstin E, Schones DE, Huang W, Steven de Belle J, . Transgenerational programming of longevity through E(z)-mediated histone H3K27 trimethylation in Drosophila. . 8:2988-3008. https://doi.org/10.18632/aging.101107

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Xia, Brian 
 AU - Gerstin, Ed 
 AU - Schones, Dustin E. 
 AU - Huang, Wendong 
 AU - Steven de Belle, J. 
 TI - Transgenerational programming of longevity through E(z)-mediated histone H3K27 trimethylation in Drosophila
 JO - 
 JA - 
 VL - 8
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101107
 DO - 10.18632/aging.101107
 SP - 2988
 EP - 3008
 PY - 
 AB - Transgenerational effects on health and development of early-life nutrition have gained increased attention recently. However, the underlying mechanisms of transgenerational transmission are only starting to emerge, with epigenetics as perhaps the most important mechanism. We recently reported the first animal model to study transgenerational programming of longevity after early-life dietary manipulations, enabling investigations to identify underlying epigenetic mechanisms. We report here that post-eclosion dietary manipulation (PDM) with a low-protein (LP) diet upregulates the protein level of E(z), an H3K27 specific methyltransferase, leading to higher levels of H3K27 trimethylation (H3K27me3). This PDM-mediated change in H3K27me3 corresponded with a shortened longevity of F0 flies as well as their F2 offspring. Specific RNAi-mediated post-eclosion knockdown of E(z) or pharmacological inhibition of its enzymatic function with EPZ-6438 in the F0 parents improved longevity while rendering H3K27me3 low across generations. Importantly, addition of EPZ-6438 to the LP diet fully alleviated the longevity-reducing effect of the LP PDM, supporting the increased level of E(z)-dependent H3K27me3 as the primary cause and immediate early-life period as the critical time to program longevity through epigenetic regulation. These observations establish E(z)-mediated H3K27me3 as one epigenetic mechanism underlying nutritional programming of longevity and support the use of EPZ-6438 to extend lifespan.
 ER -

Click to copy this citation from the text box above or download the citation:

Nickel chloride (NiCl2) in hepatic toxicity: apoptosis, G2/M cell cycle arrest and inflammatory response

Hongrui Guo, Hengmin Cui, Jing Fang, Zhicai Zuo, Junliang Deng, Xun Wang, Ling Zhao, Kejie Chen, Jie Deng,

https://doi.org/10.18632/aging.101108 pp 3009—3027

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Guo H, Cui H, Fang J, Zuo Z, Deng J, Wang X, Zhao L, Chen K, Deng J, . Nickel chloride (NiCl2) in hepatic toxicity: apoptosis, G2/M cell cycle arrest and inflammatory response. . 8:3009-3027. https://doi.org/10.18632/aging.101108

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Guo, Hongrui 
                AU  - Cui, Hengmin 
                AU  - Fang, Jing 
                AU  - Zuo, Zhicai 
                AU  - Deng, Junliang 
                AU  - Wang, Xun 
                AU  - Zhao, Ling 
                AU  - Chen, Kejie 
                AU  - Deng, Jie 
                TI  - Nickel chloride (NiCl2) in hepatic toxicity: apoptosis, G2/M cell cycle arrest and inflammatory response
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101108
                DO  - 10.18632/aging.101108
                SP  - 3009
                EP  - 3027
                PY  - 
                AB  - Up to now, the precise mechanism of Ni toxicology is still indistinct. Our aim was to test the apoptosis, cell cycle arrest and inflammatory response mechanism induced by NiCl2 in the liver of broiler chickens. NiCl2 significantly increased hepatic apoptosis. NiCl2 activated mitochondria-mediated apoptotic pathway by decreasing Bcl-2, Bcl-xL, Mcl-1, and increasing Bax, Bak, caspase-3, caspase-9 and PARP mRNA expression. In the Fas-mediated apoptotic pathway, mRNA expression levels of Fas, FasL, caspase-8 were increased. Also,NiCl2 induced ER stress apoptotic pathway by increasing GRP78 and GRP94 mRNA expressions. The ER stress was activated through PERK, IRE1 and ATF6 pathways, which were characterized by increasing eIF2α, ATF4, IRE1, XBP1 and ATF6 mRNA expressions. And, NiCl2 arrested G2/M phase cell cycle by increasing p53, p21 and decreasing cdc2, cyclin B mRNA expressions. Simultaneously, NiCl2 increased TNF-α, IL-1β, IL-6, IL-8 mRNA expressions through NF-κB activation. In conclusion, NiCl2 induces apoptosis through mitochondria, Fas and ER stress-mediated apoptotic pathways and causes cell cycle G2/M phase arrest via p53-dependent pathway and generates inflammatory response by activating NF-κB pathway.
                ER  -

Click to copy this citation from the text box above or download the citation:

Rpd3 interacts with insulin signaling in Drosophila longevity extension

Jared K. Woods, Tahereh Ziafazeli, Blanka Rogina,

https://doi.org/10.18632/aging.101110 pp 3028—3044

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Woods JK, Ziafazeli T, Rogina B, . Rpd3 interacts with insulin signaling in Drosophila longevity extension. . 8:3028-3044. https://doi.org/10.18632/aging.101110

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
 TY - JOUR
 AU - Woods, Jared K. 
 AU - Ziafazeli, Tahereh 
 AU - Rogina, Blanka 
 TI - Rpd3 interacts with insulin signaling in Drosophila longevity extension
 JO - 
 JA - 
 VL - 8
 IS - 11
 PB - 
 SN - 
 UR - https://doi.org/10.18632/aging.101110
 DO - 10.18632/aging.101110
 SP - 3028
 EP - 3044
 PY - 
 AB - Histone deacetylase (HDAC) 1 regulates chromatin compaction and gene expression by removing acetyl groups from lysine residues within histones. HDAC1 affects a variety of processes including proliferation, development, metabolism, and cancer. Reduction or inhibition of Rpd3, yeast and fly HDAC1 orthologue, extends longevity. However, the mechanism of rpd3’s effects on longevity remains unclear. Here we report an overlap between rpd3 and the Insulin/Insulin-like growth factor signaling (IIS) longevity pathways. We demonstrated that rpd3 reduction downregulates expression of members of the IIS pathway, which is associated with altered metabolism, increased energy storage, and higher resistance to starvation and oxidative stress. Genetic studies support the role of IIS in rpd3 longevity pathway, as illustrated with reduced stress resistance and longevity of flies double mutant for rpd3 and dfoxo, a downstream target of IIS pathway, compared to rpd3 single mutant flies. Our data suggest that increased dfoxo is a mediator of rpd3’s effects on fly longevity and intermediary metabolism, and confer a new link between rpd3 and IIS longevity pathways.
 ER -

Click to copy this citation from the text box above or download the citation:

On the heterogeneity of human populations as reflected by mortality dynamics

Demetris Avraam, Séverine Arnold, Olga Vasieva, Bakhtier Vasiev,

https://doi.org/10.18632/aging.101112 pp 3045—3064

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Avraam D, Arnold S, Vasieva O, Vasiev B, . On the heterogeneity of human populations as reflected by mortality dynamics. . 8:3045-3064. https://doi.org/10.18632/aging.101112

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Avraam, Demetris 
                AU  - Arnold, Séverine 
                AU  - Vasieva, Olga 
                AU  - Vasiev, Bakhtier 
                TI  - On the heterogeneity of human populations as reflected by mortality dynamics
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101112
                DO  - 10.18632/aging.101112
                SP  - 3045
                EP  - 3064
                PY  - 
                AB  - The heterogeneity of populations is used to explain the variability of mortality rates across the lifespan and their deviations from an exponential growth at young and very old ages. A mathematical model that combines the heterogeneity with the assumption that the mortality of each constituent subpopulation increases exponentially with age, has been shown to successfully reproduce the entire mortality pattern across the lifespan and its evolution over time. In this work we aim to show that the heterogeneity is not only a convenient consideration for fitting mortality data but is indeed the actual structure of the population as reflected by the mortality dynamics over age and time. In particular, we show that the model of heterogeneous population fits mortality data better than other commonly used mortality models. This was demonstrated using cohort data taken for the entire lifespan as well as for only old ages. Also, we show that the model can reproduce seemingly contradicting observations in late-life mortality dynamics. Finally, we show that the homogenisation of a population, observed by fitting the model to actual data of consecutive periods, can be associated with the evolution of allele frequencies if the heterogeneity is assumed to reflect the genetic variations within the population.
                ER  -

Click to copy this citation from the text box above or download the citation:

Mast cells and histamine are triggering the NF-κB-mediated reactions of adult and aged perilymphatic mesenteric tissues to acute inflammation

Irina Tsoy Nizamutdinova, Giuseppina F. Dusio, Olga Yu. Gasheva, Hunter Skoog, Richard Tobin, Chander Peddaboina, Cynthia J. Meininger, David C. Zawieja, M. Karen Newell-Rogers, Anatoliy A. Gashev,

https://doi.org/10.18632/aging.101113 pp 3065—3090

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Nizamutdinova IT, Dusio GF, Gasheva OY, Skoog H, Tobin R, Peddaboina C, Meininger CJ, Zawieja DC, Newell-Rogers MK, Gashev AA, . Mast cells and histamine are triggering the NF-κB-mediated reactions of adult and aged perilymphatic mesenteric tissues to acute inflammation. . 8:3065-3090. https://doi.org/10.18632/aging.101113

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Nizamutdinova, Irina Tsoy 
                AU  - Dusio, Giuseppina F. 
                AU  - Gasheva, Olga Yu. 
                AU  - Skoog, Hunter 
                AU  - Tobin, Richard 
                AU  - Peddaboina, Chander 
                AU  - Meininger, Cynthia J. 
                AU  - Zawieja, David C. 
                AU  - Newell-Rogers, M. Karen 
                AU  - Gashev, Anatoliy A. 
                TI  - Mast cells and histamine are triggering the NF-κB-mediated reactions of adult and aged perilymphatic mesenteric tissues to acute inflammation
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101113
                DO  - 10.18632/aging.101113
                SP  - 3065
                EP  - 3090
                PY  - 
                AB  - This study aimed to establish mechanistic links between the aging-associated changes in the functional status of mast cells and the altered responses of mesenteric tissue and mesenteric lymphatic vessels (MLVs) to acute inflammation. We used an in vivo model of acute peritoneal inflammation induced by lipopolysaccharide treatment of adult (9-month) and aged (24-month) F-344 rats. We analyzed contractility of isolated MLVs, mast cell activation, activation of nuclear factor-κB (NF-κB) without and with stabilization of mast cells by cromolyn or blockade of all types of histamine receptors and production of 27 major pro-inflammatory cytokines in adult and aged perilymphatic mesenteric tissues and blood. We found that the reactivity of aged contracting lymphatic vessels to LPS-induced acute inflammation was abolished and that activated mast cells trigger NF-κB signaling in the mesentery through release of histamine. The aging-associated basal activation of mesenteric mast cells limits acute inflammatory NF-κB activation in aged mesentery. We conclude that proper functioning of the mast cell/histamine/NF-κB axis is necessary for reactions of the lymphatic vessels to acute inflammatory stimuli as well as for interaction and trafficking of immune cells near and within the collecting lymphatics.
                ER  -

Click to copy this citation from the text box above or download the citation:

The role of club cell phenoconversion and migration in idiopathic pulmonary fibrosis

Jutaro Fukumoto, Ramani Soundararajan, Joseph Leung, Ruan Cox Jr., Sanjay Mahendrasah, Neha Muthavarapu, Travis Herrin, Alexander Czachor, Lee C. Tan, Nima Hosseinian, Priyanshi Patel, Jayanthraj Gone, Mason T. Breitzig, Young Cho, Andrew J. Cooke, Lakshmi Galam, Venkata Ramireddy Narala, Yashwant Pathak, Richard F. Lockey, Narasaiah Kolliputi,

https://doi.org/10.18632/aging.101115 pp 3091—3109

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Fukumoto J, Soundararajan R, Leung J, Cox R, Mahendrasah S, Muthavarapu N, Herrin T, Czachor A, Tan LC, Hosseinian N, Patel P, Gone J, Breitzig MT, et al, . The role of club cell phenoconversion and migration in idiopathic pulmonary fibrosis. . 8:3091-3109. https://doi.org/10.18632/aging.101115

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Fukumoto, Jutaro 
                AU  - Soundararajan, Ramani 
                AU  - Leung, Joseph 
                AU  - Cox, Ruan 
                AU  - Mahendrasah, Sanjay 
                AU  - Muthavarapu, Neha 
                AU  - Herrin, Travis 
                AU  - Czachor, Alexander 
                AU  - Tan, Lee C. 
                AU  - Hosseinian, Nima 
                AU  - Patel, Priyanshi 
                AU  - Gone, Jayanthraj 
                AU  - Breitzig, Mason T. 
                AU  - Cho, Young 
                AU  - Cooke, Andrew J. 
                AU  - Galam, Lakshmi 
                AU  - Narala, Venkata Ramireddy 
                AU  - Pathak, Yashwant 
                AU  - Lockey, Richard F. 
                AU  - Kolliputi, Narasaiah 
                TI  - The role of club cell phenoconversion and migration in idiopathic pulmonary fibrosis
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101115
                DO  - 10.18632/aging.101115
                SP  - 3091
                EP  - 3109
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - Fukumoto, Jutaro 
                AU  - Soundararajan, Ramani 
                AU  - Leung, Joseph 
                AU  - Cox, Ruan 
                AU  - Mahendrasah, Sanjay 
                AU  - Muthavarapu, Neha 
                AU  - Herrin, Travis 
                AU  - Czachor, Alexander 
                AU  - Tan, Lee C. 
                AU  - Hosseinian, Nima 
                AU  - Patel, Priyanshi 
                AU  - Gone, Jayanthraj 
                AU  - Breitzig, Mason T. 
                AU  - Cho, Young 
                AU  - Cooke, Andrew J. 
                AU  - Galam, Lakshmi 
                AU  - Narala, Venkata Ramireddy 
                AU  - Pathak, Yashwant 
                AU  - Lockey, Richard F. 
                AU  - Kolliputi, Narasaiah 
                TI  - The role of club cell phenoconversion and migration in idiopathic pulmonary fibrosis
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101115
                DO  - 10.18632/aging.101115
                SP  - 3091
                EP  - 3109
                PY  - 
                AB  - Idiopathic pulmonary fibrosis (IPF) is an age-related multifactorial disease featuring non-uniform lung fibrosis. The decisive cellular events at early stages of IPF are poorly understood. While the involvement of club cells in IPF pathogenesis is unclear, their migration has been associated with lung fibrosis. In this study, we labeled club cells immunohistochemically in IPF lungs using a club cell marker Claudin-10 (Cldn10), a unique protein based on the recent report which demonstrated that the appearance of Cldn10 in developing and repairing lungs precedes other club cell markers including club cell secretory protein (CCSP). Cldn10-positive cells in IPF lungs displayed marked pleomorphism and were found in varied arrangements, suggesting their phenoconversion. These results were corroborated by immunogold labeling for Cldn10. Further, immunohistochemical double-labeling for Cldn10 and α-smooth muscle actin (α-SMA) demonstrated that aberrant α-SMA signals are frequently encountered near disorganized Cldn10-positive cells in hyperplastic bronchiolar epithelium and thickened interstitium of IPF lungs. Collectively, these data indicate that club cells actively participate in the initiation and progression of IPF through phenoconversion involving the acquisition of proliferative and migratory abilities. Thus, our new findings open the possibility for club cell-targeted therapy to become a strategic option for the treatment of IPF.
                ER  -

Click to copy this citation from the text box above or download the citation:

Immune function parameters as markers of biological age and predictors of longevity

Irene Martínez de Toda, Ianire Maté, Carmen Vida, Julia Cruces, Mónica De la Fuente,

https://doi.org/10.18632/aging.101116 pp 3110—3119

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Martínez de Toda I, Maté I, Vida C, Cruces J, De la Fuente M, . Immune function parameters as markers of biological age and predictors of longevity. . 8:3110-3119. https://doi.org/10.18632/aging.101116

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Martínez de Toda, Irene 
                AU  - Maté, Ianire 
                AU  - Vida, Carmen 
                AU  - Cruces, Julia 
                AU  - De la Fuente, Mónica 
                TI  - Immune function parameters as markers of biological age and predictors of longevity
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101116
                DO  - 10.18632/aging.101116
                SP  - 3110
                EP  - 3119
                PY  - 
                AB  - Chronological age is not a good indicator of how each individual ages and thus how to maintain good health. Due to the long lifespan in humans and the consequent difficulty of carrying out longitudinal studies, finding valid biomarkers of the biological age has been a challenge both for research and clinical studies. The aim was to identify and validate several immune cell function parameters as markers of biological age. Adult, mature, elderly and long-lived human volunteers were used. The chemotaxis, phagocytosis, natural killer activity and lymphoproliferation in neutrophils and lymphocytes of peripheral blood were analyzed. The same functions were measured in peritoneal immune cells from mice, at the corresponding ages (adult, mature, old and long lived) in a longitudinal study. The results showed that the evolution of these functions was similar in humans and mice, with a decrease in old subjects. However, the long-lived individuals maintained values similar to those in adults. In addition, the values of these functions in adult prematurely aging mice were similar to those in chronologically old animals, and they died before their non-prematurely aging mice counterparts. Thus, the parameters studied are good markers of the rate of aging, allowing the determination of biological age.
                ER  -

Click to copy this citation from the text box above or download the citation:

Rapamycin treatment benefits glucose metabolism in mouse models of type 2 diabetes

Peter C. Reifsnyder, Kevin Flurkey, Austen Te, David E. Harrison,

https://doi.org/10.18632/aging.101117 pp 3120—3130

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Reifsnyder PC, Flurkey K, Te A, Harrison DE, . Rapamycin treatment benefits glucose metabolism in mouse models of type 2 diabetes. . 8:3120-3130. https://doi.org/10.18632/aging.101117

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Reifsnyder, Peter C. 
                AU  - Flurkey, Kevin 
                AU  - Te, Austen 
                AU  - Harrison, David E. 
                TI  - Rapamycin treatment benefits glucose metabolism in mouse models of type 2 diabetes
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101117
                DO  - 10.18632/aging.101117
                SP  - 3120
                EP  - 3130
                PY  - 
                AB  - Numerous studies suggest that rapamycin treatment promotes insulin resistance, implying that rapamycin could have negative effects on patients with, or at risk for, type 2 diabetes (T2D). New evidence, however, indicates that rapamycin treatment produces some benefits to energy metabolism, even in the context of T2D. Here, we survey 5 mouse models of T2D (KK, KK-Ay, NONcNZO10, BKS-db/db, TALLYHO) to quantify effects of rapamycin on well-recognized markers of glucose homeostasis within a wide range of T2D environments. Interestingly, dietary rapamycin treatment did not exacerbate impaired glucose or insulin tolerance, or elevate circulating lipids as T2D progressed. In fact, rapamycin increased insulin sensitivity and reduced weight gain in 3 models, and decreased hyperinsulinemia in 2 models. A key covariate of this genetically-based, differential response was pancreatic insulin content (PIC): Models with low PIC exhibited more beneficial effects than models with high PIC. However, a minimal PIC threshold may exist, below which hypoinsulinemic hyperglycemia develops, as it did in TALLYHO. Our results, along with other studies, indicate that beneficial or detrimental metabolic effects of rapamycin treatment, in a diabetic or pre-diabetic context, are driven by the interaction of rapamycin with the individual model’s pancreatic physiology.
                ER  -

Click to copy this citation from the text box above or download the citation:

Early age decline in DNA repair capacity in the liver: in depth profile of differential gene expression

Avital Guedj, Anat Geiger-Maor, Hadar Benyamini, Yaval Nevo, Sharona Elgavish, Eithan Galun, Hagai Amsalem, Jacob Rachmilewitz,

https://doi.org/10.18632/aging.101120 pp 3131—3146

View Abstract PDF Full-Text How to Cite Request Reprint

Cite this Article

How to cite

Guedj A, Geiger-Maor A, Benyamini H, Nevo Y, Elgavish S, Galun E, Amsalem H, Rachmilewitz J, . Early age decline in DNA repair capacity in the liver: in depth profile of differential gene expression. . 8:3131-3146. https://doi.org/10.18632/aging.101120

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Provider: 
                TY  - JOUR
                AU  - Guedj, Avital 
                AU  - Geiger-Maor, Anat 
                AU  - Benyamini, Hadar 
                AU  - Nevo, Yaval 
                AU  - Elgavish, Sharona 
                AU  - Galun, Eithan 
                AU  - Amsalem, Hagai 
                AU  - Rachmilewitz, Jacob 
                TI  - Early age decline in DNA repair capacity in the liver: in depth profile of differential gene expression
                JO  - 
                JA  - 
                VL  - 8
                IS  - 11
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.101120
                DO  - 10.18632/aging.101120
                SP  - 3131
                EP  - 3146
                PY  - 
                AB  - Aging is associated with progressive decline in cell function and with increased damage to macromolecular components. DNA damage, in the form of double-strand breaks (DSBs), increases with age and in turn, contributes to the aging process and age-related diseases. DNA strand breaks triggers a set of highly orchestrated signaling events known as the DNA damage response (DDR), which coordinates DNA repair. However, whether the accumulation of DNA damage with age is a result of decreased repair capacity, remains to be determined. In our study we showed that with age there is a decline in the resolution of foci containing γH2AX and pKAP-1 in diethylnitrosamine (DEN)-treated mouse livers, already evident at a remarkably early age of 6-months. Considerable age-dependent differences in global gene expression profiles in mice livers after exposure to DEN, further affirmed these age related differences in the response to DNA damage. Functional analysis identified p53 as the most overrepresented pathway that is specifically enhanced and prolonged in 6-month-old mice. Collectively, our results demonstrated an early decline in DNA damage repair that precedes ‘old age’, suggesting this may be a driving force contributing to the aging process rather than a phenotypic consequence of old age.
                ER  -

Click to copy this citation from the text box above or download the citation:

The Fhit protein: an opportunity to overcome chemoresistance

Eugenio Gaudio, Francesco Paduano, Carlo M. Croce, Francesco Trapasso,

https://doi.org/10.18632/aging.101123 pp 3147—3150

PDF How to Cite Request Reprint

Cite this Article

How to cite

Gaudio E, Paduano F, Croce CM, Trapasso F, . The Fhit protein: an opportunity to overcome chemoresistance. . 8:3147-3150. https://doi.org/10.18632/aging.101123

Copy or Download citation:

Select the format you require from the list below

Plain text
EndNote
Reference Manager
ProCite
BibteX

Click to copy this citation from the text box above or download the citation:

Volume 8, Issue 11

About the Cover

Editorials

Andrew D. Hollenbach,

Cite this Article

How to cite

Copy or Download citation:

Wolfgang Deppert, Michael Bruns,

Cite this Article

How to cite

Copy or Download citation:

Luca Cardone,

Cite this Article

How to cite

Copy or Download citation:

Research Papers

Ganesh V. Halade, Vasundhara Kain, Laurence M. Black, Sumanth D. Prabhu, Kevin A. Ingle,

Cite this Article

How to cite

Copy or Download citation:

Wen-Hua Qi, Chao-chao Yan, Wu-Jiao Li, Xue-Mei Jiang, Guang-Zhou Li, Xiu-Yue Zhang, Ting-Zhang Hu, Jing Li, Bi-Song Yue,

Cite this Article

How to cite

Copy or Download citation:

Carolina Soriano-Tárraga, Eva Giralt-Steinhauer, Marina Mola-Caminal, Rosa M. Vivanco-Hidalgo, Angel Ois, Ana Rodríguez-Campello, Elisa Cuadrado-Godia, Sergi Sayols-Baixeras, Roberto Elosua, Jaume Roquer, Jordi Jiménez-Conde,

Cite this Article

How to cite

Copy or Download citation:

Chan-Il Choi, Ki Hyun Yoo, Syed Mohammed Qasim Hussaini, Byeong Tak Jeon, John Welby, Haiyun Gan, Isobel A. Scarisbrick, Zhiguo Zhang, Darren J. Baker, Jan M. van Deursen, Moses Rodriguez, Mi-Hyeon Jang,

Cite this Article

How to cite

Copy or Download citation:

Wahyu Wulaningsih, Johnathan Watkins, Tetsuya Matsuguchi, Rebecca Hardy,

Cite this Article

How to cite

Copy or Download citation:

Anton M.F. Kalsbeek, Eva F.K. Chan, Judith Grogan, Desiree C. Petersen, Weerachai Jaratlerdsiri, Ruta Gupta, Ruth J. Lyons, Anne-Maree Haynes, Lisa G. Horvath, James G. Kench, Phillip D. Stricker, Vanessa M. Hayes,

Cite this Article

How to cite

Copy or Download citation:

Natalia A. Stefanova, Natalia A. Muraleva, Kseniya Yi. Maksimova, Ekaterina A. Rudnitskaya, Elena Kiseleva, Darya V. Telegina, Nataliya G. Kolosova,

Cite this Article

How to cite

Copy or Download citation:

Fei-Feng Li, Xi-Dong Zhu, Peng Yan, Mei-Hua Jin, Hui Yue, Qiong Zhang, Jin Fu, Shu-Lin Liu,

Cite this Article

How to cite

Copy or Download citation:

Elena Lopez-Guadamillas, Maribel Muñoz-Martin, Sonia Martinez, Joaquin Pastor, Pablo J. Fernandez-Marcos, Manuel Serrano,

Cite this Article

How to cite

Copy or Download citation:

Qiaoxiang Dong, Hui Gao, Yuanshuo Shi, Fuchuang Zhang, Xiang Gu, Anqi Wu, Danhan Wang, Yuanhong Chen, Abhik Bandyopadhyay, I-Tien Yeh, Benjamin J. Daniel, Yidong Chen, Yi Zou, Vivienne L. Rebel, Christi A. Walter, Jianxin Lu, Changjiang Huang, Lu-Zhe Sun,

Cite this Article

How to cite

Copy or Download citation:

Claire Rühlmann, Tjark Wölk, Tobias Blümel, Laura Stahn, Brigitte Vollmar, Angela Kuhla,

Cite this Article

How to cite

Copy or Download citation:

Xinxin Wang, Feng Liu, Xiaoyu Qin, Tinglei Huang, Bo Huang, Yanjie Zhang, Bin Jiang,

Cite this Article

How to cite

Copy or Download citation:

Lotta Kilpinen, Amarjit Parmar, Dario Greco, Matti Korhonen, Petri Lehenkari, Päivi Saavalainen, Saara Laitinen,

Cite this Article

How to cite

Copy or Download citation:

Ishita Parikh, Janet Guo, Kai-Hsiang Chuang, Yu Zhong, Ralf G. Rempe, Jared D. Hoffman, Rachel Armstrong, Björn Bauer, Anika M.S. Hartz, Ai-Ling Lin,

Cite this Article

How to cite

Copy or Download citation:

Jun Liu, Ming-Hong He, Jing Peng, Yi-Min Duan, Yi-Si Lu, Zhenfang Wu, Ting Gong, Hong-Tao Li, Jin-Qiu Zhou,

Cite this Article

How to cite

Copy or Download citation:

Veronika Borbélyová, Emese Domonkos, Janka Bábíčková, Ľubomíra Tóthová, Martin Bosý, Július Hodosy, Peter Celec,

Cite this Article

How to cite

Copy or Download citation: