Volume 8, Issue 6

Kaplon RE, Hill SD, Bispham NZ, Santos-Parker JR, Nowlan MJ, Snyder LL, Chonchol M, LaRocca TJ, McQueen MB, Seals DR, . Oral trehalose supplementation improves resistance artery endothelial function in healthy middle-aged and older adults. . 8:1167-1183. https://doi.org/10.18632/aging.100962

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                TY  - JOUR
                AU  - Kaplon, Rachelle E. 
                AU  - Hill, Sierra D. 
                AU  - Bispham, Nina Z. 
                AU  - Santos-Parker, Jessica R. 
                AU  - Nowlan, Molly J. 
                AU  - Snyder, Laura L. 
                AU  - Chonchol, Michel 
                AU  - LaRocca, Thomas J. 
                AU  - McQueen, Matthew B. 
                AU  - Seals, Douglas R. 
                TI  - Oral trehalose supplementation improves resistance artery endothelial function in healthy middle-aged and older adults
                JO  - 
                JA  - 
                VL  - 8
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100962
                DO  - 10.18632/aging.100962
                SP  - 1167
                EP  - 1183
                PY  - 
                AB  - We hypothesized that supplementation with trehalose, a disaccharide that reverses arterial aging in mice, would improve vascular function in middle-aged and older (MA/O) men and women. Thirty-two healthy adults aged 50-77 years consumed 100 g/day of trehalose (n=15) or maltose (n=17, isocaloric control) for 12 weeks (randomized, double-blind). In subjects with Δbody mass&lt;2.3kg (5 lb.), resistance artery endothelial function, assessed by forearm blood flow to brachial artery infusion of acetylcholine (FBFACh), increased ∼30% with trehalose (13.3±1.0 vs. 10.5±1.1 AUC, P=0.02), but not maltose (P=0.40). This improvement in FBFACh was abolished when endothelial nitric oxide (NO) production was inhibited. Endothelium-independent dilation, assessed by FBF to sodium nitroprusside (FBFSNP), also increased ∼30% with trehalose (155±13 vs. 116±12 AUC, P=0.03) but not maltose (P=0.92). Changes in FBFACh and FBFSNP with trehalose were not significant when subjects with Δbody mass≥2.3kg were included. Trehalose supplementation had no effect on conduit artery endothelial function, large elastic artery stiffness or circulating markers of oxidative stress or inflammation (all P&gt;0.1) independent of changes in body weight. Our findings demonstrate that oral trehalose improves resistance artery (microvascular) function, a major risk factor for cardiovascular diseases, in MA/O adults, possibly through increasing NO bioavailability and smooth muscle sensitivity to NO.
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Reduced SOD2 expression is associated with mortality of hepatocellular carcinoma patients in a mutant p53-dependent manner

Ren Wang, Chen Yin, Xiao-Xing Li, Xian-Zi Yang, Yang Yang, Mei-Yin Zhang, Hui-Yun Wang, X.F. Steven Zheng,

https://doi.org/10.18632/aging.100967 pp 1184—1200

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Wang R, Yin C, Li X, Yang X, Yang Y, Zhang M, Wang H, Zheng XS, . Reduced SOD2 expression is associated with mortality of hepatocellular carcinoma patients in a mutant p53-dependent manner. . 8:1184-1200. https://doi.org/10.18632/aging.100967

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                TY  - JOUR
                AU  - Wang, Ren 
                AU  - Yin, Chen 
                AU  - Li, Xiao-Xing 
                AU  - Yang, Xian-Zi 
                AU  - Yang, Yang 
                AU  - Zhang, Mei-Yin 
                AU  - Wang, Hui-Yun 
                AU  - Zheng, X.F. Steven
                TI  - Reduced SOD2 expression is associated with mortality of hepatocellular carcinoma patients in a mutant p53-dependent manner
                JO  - 
                JA  - 
                VL  - 8
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100967
                DO  - 10.18632/aging.100967
                SP  - 1184
                EP  - 1200
                PY  - 
                AB  - The development and progression of hepatocellular carcinoma (HCC) is accompanied with persistent oxidative stress, but the molecular basis is not well defined. Superoxide dismutase 2 (SOD2) is an important mitochondrial antioxidant and a key aging factor. Here we investigated the expression and clinical significance of SOD2 in a large cohort of HBV-positive HCC tumors. Both SOD2 mRNA and protein are reduced in human primary HCCs compared with matching liver tissues. Consistently, the SOD2 DNA copy numbers are decreased in HCCs, providing a genetic basis for the decrease in SOD2 mRNA expression. Reduced SOD2 expression in HCCs is correlated with older age, larger tumor size, multiple tumor nodules and tumor emboli, and cancer recurrence. Moreover, low SOD2 expression is strongly associated with poor overall survival (OS) and recurrence-free survival (RFS). Univariate and multivariate Cox regression analyses indicates that SOD2 is an independent prognostic predictor for OS and RFS. Intriguingly, reduced SOD2 mRNA is strongly associated with poor survival in a separate cohort of HCC patients carrying mutant p53. Altogether, our results provide clinical evidence for the importance of SOD2 in tumor progression and mortality, and the close relationship of SOD2 and p53 in HCC.
                ER  -

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Fat-specific Dicer deficiency accelerates aging and mitigates several effects of dietary restriction in mice

Felipe C. G., Jéssica L. O., Bruna B. Brandão, Beatriz A. Guerra, Ismael D. Silva, Andrea Frontini, Thomas Thomou, Loris Sartini, Saverio Cinti, C. Ronald Kahn, William T. Festuccia, Alicia J. Kowaltowski, Marcelo A. Mori,

https://doi.org/10.18632/aging.100970 pp 1201—1222

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G. FC, O. JL, Brandão BB, Guerra BA, Silva ID, Frontini A, Thomou T, Sartini L, Cinti S, Kahn CR, Festuccia WT, Kowaltowski AJ, Mori MA, . Fat-specific Dicer deficiency accelerates aging and mitigates several effects of dietary restriction in mice. . 8:1201-1222. https://doi.org/10.18632/aging.100970

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                TY  - JOUR
                AU  - G., Felipe C.
                AU  - O., Jéssica L.
                AU  - Brandão, Bruna B.
                AU  - Guerra, Beatriz A.
                AU  - Silva, Ismael D.
                AU  - Frontini, Andrea 
                AU  - Thomou, Thomas 
                AU  - Sartini, Loris 
                AU  - Cinti, Saverio 
                AU  - Kahn, C. Ronald
                AU  - Festuccia, William T.
                AU  - Kowaltowski, Alicia J.
                AU  - Mori, Marcelo A.
                TI  - Fat-specific Dicer deficiency accelerates aging and mitigates several effects of dietary restriction in mice
                JO  - 
                JA  - 
                VL  - 8
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100970
                DO  - 10.18632/aging.100970
                SP  - 1201
                EP  - 1222
                PY  - 
                ER  -

Provider: 
                TY  - JOUR
                AU  - G., Felipe C.
                AU  - O., Jéssica L.
                AU  - Brandão, Bruna B.
                AU  - Guerra, Beatriz A.
                AU  - Silva, Ismael D.
                AU  - Frontini, Andrea 
                AU  - Thomou, Thomas 
                AU  - Sartini, Loris 
                AU  - Cinti, Saverio 
                AU  - Kahn, C. Ronald
                AU  - Festuccia, William T.
                AU  - Kowaltowski, Alicia J.
                AU  - Mori, Marcelo A.
                TI  - Fat-specific Dicer deficiency accelerates aging and mitigates several effects of dietary restriction in mice
                JO  - 
                JA  - 
                VL  - 8
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100970
                DO  - 10.18632/aging.100970
                SP  - 1201
                EP  - 1222
                PY  - 
                AB  - Aging increases the risk of type 2 diabetes, and this can be prevented by dietary restriction (DR). We have previously shown that DR inhibits the downregulation of miRNAs and their processing enzymes - mainly Dicer - that occurs with aging in mouse white adipose tissue (WAT). Here we used fat-specific Dicer knockout mice (AdicerKO) to understand the contributions of adipose tissue Dicer to the metabolic effects of aging and DR. Metabolomic data uncovered a clear distinction between the serum metabolite profiles of Lox control and AdicerKO mice, with a notable elevation of branched-chain amino acids (BCAA) in AdicerKO. These profiles were associated with reduced oxidative metabolism and increased lactate in WAT of AdicerKO mice and were accompanied by structural and functional changes in mitochondria, particularly under DR. AdicerKO mice displayed increased mTORC1 activation in WAT and skeletal muscle, where Dicer expression is not affected. This was accompanied by accelerated age-associated insulin resistance and premature mortality. Moreover, DR-induced insulin sensitivity was abrogated in AdicerKO mice. This was reverted by rapamycin injection, demonstrating that insulin resistance in AdicerKO mice is caused by mTORC1 hyperactivation. Our study evidences a DR-modulated role for WAT Dicer in controlling metabolism and insulin resistance.
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Retinoic acid treated human dendritic cells induce T regulatory cells via the expression of CD141 and GARP which is impaired with age

Sudhanshu Agrawal, Sreerupa Ganguly, Alexander Tran, Padmaja Sundaram, Anshu Agrawal,

https://doi.org/10.18632/aging.100973 pp 1223—1235

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Agrawal S, Ganguly S, Tran A, Sundaram P, Agrawal A, . Retinoic acid treated human dendritic cells induce T regulatory cells via the expression of CD141 and GARP which is impaired with age. . 8:1223-1235. https://doi.org/10.18632/aging.100973

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                TY  - JOUR
                AU  - Agrawal, Sudhanshu 
                AU  - Ganguly, Sreerupa 
                AU  - Tran, Alexander 
                AU  - Sundaram, Padmaja 
                AU  - Agrawal, Anshu 
                TI  - Retinoic acid treated human dendritic cells induce T regulatory cells via the expression of CD141 and GARP which is impaired with age
                JO  - 
                JA  - 
                VL  - 8
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100973
                DO  - 10.18632/aging.100973
                SP  - 1223
                EP  - 1235
                PY  - 
                AB  - Aged subjects display increased susceptibility to mucosal diseases. Retinoic Acid (RA) plays a major role in inducing tolerance in the mucosa. RA acts on Dendritic cells (DCs) to induce mucosal tolerance.  Here we compared the response of DCs from aged and young individuals to RA with a view to understand the role of DCs in age-associated increased susceptibility to mucosal diseases. Our investigations revealed that compared to young DCs, RA stimulated DCs from aged subjects are defective in inducing IL-10 and T regulatory cells.  Examinations of the underlying mechanisms indicated that RA exposure led to the upregulation of CD141 and GARP on DCs which rendered the DCs tolerogenic. CD141hi, GARP+ DCs displayed enhanced capacity to induce T regulatory cells compared to CD141lo and GARP- DCs. Unlike RA stimulated DCs from young, DCs from aged subjects exhibited diminished upregulation of both CD141 and GARP. The percentage of DCs expressing CD141 and GARP on RA treatment was significantly reduced in DCs from aged individuals. Furthermore, the remaining CD141hi, GARP+ DCs from aged individuals were also deficient in inducing T regs. In summary, reduced response of aged DCs to RA enhances mucosal inflammation in the elderly, increasing their susceptibility to mucosal diseases.
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Overexpressed HDAC4 is associated with poor survival and promotes tumor progression in esophageal carcinoma

Li-Si Zeng, Xian-Zi Yang, Yue-Feng Wen, Shi-Juan Mai, Meng-He Wang, Mei-Yin Zhang, X.F. Steven Zheng, Hui-Yun Wang,

https://doi.org/10.18632/aging.100980 pp 1236—1248

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Zeng L, Yang X, Wen Y, Mai S, Wang M, Zhang M, Zheng XS, Wang H, . Overexpressed HDAC4 is associated with poor survival and promotes tumor progression in esophageal carcinoma. . 8:1236-1248. https://doi.org/10.18632/aging.100980

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                TY  - JOUR
                AU  - Zeng, Li-Si 
                AU  - Yang, Xian-Zi 
                AU  - Wen, Yue-Feng 
                AU  - Mai, Shi-Juan 
                AU  - Wang, Meng-He 
                AU  - Zhang, Mei-Yin 
                AU  - Zheng, X.F. Steven 
                AU  - Wang, Hui-Yun 
                TI  - Overexpressed HDAC4 is associated with poor survival and promotes tumor progression in esophageal carcinoma
                JO  - 
                JA  - 
                VL  - 8
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100980
                DO  - 10.18632/aging.100980
                SP  - 1236
                EP  - 1248
                PY  - 
                AB  - Histone deacetylases (HDACs) mediate histone deacetylation, leading to transcriptional repression, which is involved in many diseases, including age-related tissue degeneration, heart failure and cancer. In this study, we were aimed to investigate the expression, clinical significance and biological function of HDAC4 in esophageal carcinoma (EC). We found that HDAC4 mRNA and protein are overexpressed in esophageal squamous cell carcinoma (ESCC) tissues and cell lines. HDAC4 overexpression is associated with higher tumor grade, advanced clinical stage and poor survival. Mechanistically, HDAC4 promotes proliferation and G1/S cell cycle progression in EC cells by inhibiting cyclin-dependent kinase (CDK) inhibitors p21 and p27 and up-regulating CDK2/4 and CDK-dependent Rb phosphorylation. HDAC4 also enhances ESCC cell migration. Furthermore, HDAC4 positively regulates epithelial-mesenchymal transition (EMT) by increasing the expression of Vimentin and decreasing the expression of E-Cadherin/α-Catenin. Together, our study shows that HDAC4 overexpression is important for the oncogenesis of EC, which may serve as a useful prognostic biomarker and therapeutic target for this malignancy.
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Reversal of cognitive decline in Alzheimer's disease

Dale E. Bredesen, Edwin C. Amos, Jonathan Canick, Mary Ackerley, Cyrus Raji, Milan Fiala, Jamila Ahdidan,

https://doi.org/10.18632/aging.100981 pp 1250—1258

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Bredesen DE, Amos EC, Canick J, Ackerley M, Raji C, Fiala M, Ahdidan J, . Reversal of cognitive decline in Alzheimer's disease. . 8:1250-1258. https://doi.org/10.18632/aging.100981

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                TY  - JOUR
                AU  - Bredesen, Dale E.
                AU  - Amos, Edwin C.
                AU  - Canick, Jonathan 
                AU  - Ackerley, Mary 
                AU  - Raji, Cyrus 
                AU  - Fiala, Milan 
                AU  - Ahdidan, Jamila 
                TI  - Reversal of cognitive decline in Alzheimer's disease
                JO  - 
                JA  - 
                VL  - 8
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100981
                DO  - 10.18632/aging.100981
                SP  - 1250
                EP  - 1258
                PY  - 
                AB  - Alzheimer's disease is one of the most significant healthcare problems nationally and globally. Recently, the first description of the reversal of cognitive decline in patients with early Alzheimer's disease or its precursors, MCI (mild cognitive impairment) and SCI (subjective cognitive impairment), was published [1]. The therapeutic approach used was programmatic and personalized rather than monotherapeutic and invariant, and was dubbed metabolic enhancement for neurodegeneration (MEND). Patients who had had to discontinue work were able to return to work, and those struggling at work were able to improve their performance. The patients, their spouses, and their co-workers all reported clear improvements. Here we report the results from quantitative MRI and neuropsychological testing in ten patients with cognitive decline, nine ApoE4+ (five homozygous and four heterozygous) and one ApoE4-, who were treated with the MEND protocol for 5-24 months. The magnitude of the improvement is unprecedented, providing additional objective evidence that this programmatic approach to cognitive decline is highly effective. These results have far-reaching implications for the treatment of Alzheimer's disease, MCI, and SCI; for personalized programs that may enhance pharmaceutical efficacy; and for personal identification of ApoE genotype.
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Growth differentiation factor 6 derived from mesenchymal stem/stromal cells reduces age-related functional deterioration in multiple tissues

Daisuke Hisamatsu, Michiko Ohno-Oishi, Shiho Nakamura, Yo Mabuchi, Hayato Naka-Kaneda,

https://doi.org/10.18632/aging.100982 pp 1259—1275

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Hisamatsu D, Ohno-Oishi M, Nakamura S, Mabuchi Y, Naka-Kaneda H, . Growth differentiation factor 6 derived from mesenchymal stem/stromal cells reduces age-related functional deterioration in multiple tissues. . 8:1259-1275. https://doi.org/10.18632/aging.100982

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                TY  - JOUR
                AU  - Hisamatsu, Daisuke 
                AU  - Ohno-Oishi, Michiko 
                AU  - Nakamura, Shiho 
                AU  - Mabuchi, Yo 
                AU  - Naka-Kaneda, Hayato 
                TI  - Growth differentiation factor 6 derived from mesenchymal stem/stromal cells reduces age-related functional deterioration in multiple tissues
                JO  - 
                JA  - 
                VL  - 8
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100982
                DO  - 10.18632/aging.100982
                SP  - 1259
                EP  - 1275
                PY  - 
                AB  - The senescence-associated secretory phenotype (SASP) has attracted attention as a mechanism that connects cellular senescence to tissue dysfunction, and specific SASP factors have been identified as systemic pro-aging factors. However, little is known about the age-dependent changes in the secretory properties of stem cells. Young, but not old, mesenchymal stem/stromal cells (MSCs) are a well-known source of critical regenerative factors, but the identity of these factors remains elusive. In this study, we identified growth differentiation factor 6 (Gdf6; also known as Bmp13 and CDMP-2) as a regenerative factor secreted from young MSCs. The expression of specific secretory factors, including Gdf6, was regulated by the microRNA (miRNA) miR-17, whose expression declined with age. Upregulation of Gdf6 restored the osteogenic capacity of old MSCs in vitro and exerted positive effects in vivo on aging-associated pathologies such as reduced lymphopoiesis, insufficient muscle repair, reduced numbers of neural progenitors in the brain, and chronic inflammation. Our results suggest that manipulation of miRNA could enable control of the SASP, and that regenerative factors derived from certain types of young cells could be used to treat geriatric diseases.
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ERP44 inhibits human lung cancer cell migration mainly via IP3R2

Xue Huang, Meng Jin, Ying-Xiao Chen, Jun Wang, Yan Chang, Qi Yuan, Kai-Tai Yao, Guangju Ji,

https://doi.org/10.18632/aging.100984 pp 1276—1286

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Huang X, Jin M, Chen Y, Wang J, Chang Y, Yuan Q, Yao K, Ji G, . ERP44 inhibits human lung cancer cell migration mainly via IP3R2. . 8:1276-1286. https://doi.org/10.18632/aging.100984

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                TY  - JOUR
                AU  - Huang, Xue 
                AU  - Jin, Meng 
                AU  - Chen, Ying-Xiao 
                AU  - Wang, Jun 
                AU  - Chang, Yan 
                AU  - Yuan, Qi 
                AU  - Yao, Kai-Tai 
                AU  - Ji, Guangju 
                TI  - ERP44 inhibits human lung cancer cell migration mainly via IP3R2
                JO  - 
                JA  - 
                VL  - 8
                IS  - 6
                PB  - 
                SN  - 
                UR  - https://doi.org/10.18632/aging.100984
                DO  - 10.18632/aging.100984
                SP  - 1276
                EP  - 1286
                PY  - 
                AB  - Cancer cell migration is involved in tumour metastasis. However, the relationship between calcium signalling and cancer migration is not well elucidated. In this study, we used the human lung adenocarcinoma A549 cell line to examine the role of endoplasmic reticulum protein 44 (ERP44), which has been reported to regulate calcium release inside of the endoplasmic reticulum (ER), in cell migration. We found that the inositol 1,4,5-trisphosphate receptors (IP3Rs/ITPRs) inhibitor 2-APB significantly inhibited A549 cell migration by inhibiting cell polarization and pseudopodium protrusion, which suggests that Ca2+ is necessary for A549 cell migration. Similarly, the overexpression of ERP44 reduced intracellular Ca2+ release via IP3Rs, altered cell morphology and significantly inhibited the migration of A549 cells. These phenomena were primarily dependent on IP3R2 because wound healing in A549 cells with IP3R2 rather than IP3R1 or IP3R3 siRNA was markedly inhibited. Moreover, the overexpression of ERP44 did not affect the migration of the human neuroblastoma cell line SH-SY5Y, which mainly expresses IP3R1. Based on the above observations, we conclude that ERP44 regulates A549 cell migration mainly via an IP3R2-dependent pathway.
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Volume 8, Issue 6

About the Cover

Editorials

Targeting mutant p53 for cancer therapy

Moshe Oren, Perry Tal, Varda Rotter,

Zinc intake, microRNA dysregulation, and esophageal cancer

Louise Y. Fong, John L. Farber, Carlo M. Croce,

Aging: T cell metabolism within tumors

Ying Zhang, Hildegund CJ Ertl,

mTORC1 regulates nutrient access in Ras-mediated tumors

Heesun Cheong,

Research Papers

Oral trehalose supplementation improves resistance artery endothelial function in healthy middle-aged and older adults

Rachelle E. Kaplon, Sierra D. Hill, Nina Z. Bispham, Jessica R. Santos-Parker, Molly J. Nowlan, Laura L. Snyder, Michel Chonchol, Thomas J. LaRocca, Matthew B. McQueen, Douglas R. Seals,

Reduced SOD2 expression is associated with mortality of hepatocellular carcinoma patients in a mutant p53-dependent manner

Ren Wang, Chen Yin, Xiao-Xing Li, Xian-Zi Yang, Yang Yang, Mei-Yin Zhang, Hui-Yun Wang, X.F. Steven Zheng,

Fat-specific Dicer deficiency accelerates aging and mitigates several effects of dietary restriction in mice

Felipe C. G., Jéssica L. O., Bruna B. Brandão, Beatriz A. Guerra, Ismael D. Silva, Andrea Frontini, Thomas Thomou, Loris Sartini, Saverio Cinti, C. Ronald Kahn, William T. Festuccia, Alicia J. Kowaltowski, Marcelo A. Mori,

Retinoic acid treated human dendritic cells induce T regulatory cells via the expression of CD141 and GARP which is impaired with age

Sudhanshu Agrawal, Sreerupa Ganguly, Alexander Tran, Padmaja Sundaram, Anshu Agrawal,

Overexpressed HDAC4 is associated with poor survival and promotes tumor progression in esophageal carcinoma

Li-Si Zeng, Xian-Zi Yang, Yue-Feng Wen, Shi-Juan Mai, Meng-He Wang, Mei-Yin Zhang, X.F. Steven Zheng, Hui-Yun Wang,

Reversal of cognitive decline in Alzheimer's disease

Dale E. Bredesen, Edwin C. Amos, Jonathan Canick, Mary Ackerley, Cyrus Raji, Milan Fiala, Jamila Ahdidan,

Growth differentiation factor 6 derived from mesenchymal stem/stromal cells reduces age-related functional deterioration in multiple tissues

Daisuke Hisamatsu, Michiko Ohno-Oishi, Shiho Nakamura, Yo Mabuchi, Hayato Naka-Kaneda,

ERP44 inhibits human lung cancer cell migration mainly via IP3R2

Xue Huang, Meng Jin, Ying-Xiao Chen, Jun Wang, Yan Chang, Qi Yuan, Kai-Tai Yao, Guangju Ji,

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