Research Paper Volume 12, Issue 20 pp 20001—20023

Figure 4. Ccl2 overexpression significantly altered the expression of the complexes related to oxidative phosphorylation and the relevant metabolic signaling pathways in the quadriceps muscle. Ccl2 overexpression exacerbated the metabolic reduction, mainly in mitochondria, (A) of the mice with accelerated aging and altered (B) the functioning of AMPK-mTOR-driven pathways. LMNAG609G/+;CGCCL2+/- and LMNAG609G/+ denote progeroid mice overexpressing and not overexpressing Ccl2, respectively. Values are shown as the means ± SEM; ^a p< 0.05 with respect to the wild-type mice and ^b p<0.05 with respect to the LMNAG609G/+ mice according to the Mann–Whitney U tests. Acronyms in (A) denote complex I or NADH/ubiquinone oxidoreductase, complex II or succinate dehydrogenase, complex III or cytochrome C reductase, complex IV or cytochrome C oxidase, complex V or ATP synthase, translocase of outer membrane (TOM20), and mitofusin 2 (Mfn2); acronyms in (B) phospho-tumor suppressor p53 (p53-pS15), tumor suppressor p53 (P53), phosphoinositide 3-kinase (PI3K), protein kinase B (AKT) and phospho-protein kinase B (AKT-pS473), phospho-ribosomal protein S6 (S6-pS235/236), ribosomal protein S6 (S6), AMPK activated protein kinase (AMPK), phospho-AMPK activated protein kinase (AMPK pT172), microtubule-associated proteins 1A/1B light chain 3B (LC3), p62 adaptor protein or sequestosome 1, and lysosome-associated membrane protein 2 (LAMP2A).