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. Author manuscript; available in PMC: 2021 Aug 11.
Published in final edited form as: Nat Aging. 2021 Feb 11;1(2):205–217. doi: 10.1038/s43587-021-00027-5

Figure 6: SIRT3 deficiency induces fibroblast senescence and resistance to apoptosis and upregulates pro-fibrotic markers.

Figure 6:

(a) Human lung fibroblasts (IMR-90) were treated with non-targeting or SIRT3 siRNA, and analyzed by western blot analysis for SIRT3, p16, phospho-Rb, total-Rb and PCNA levels. (b-e) Quantitative analysis of SIRT3 (n = 3), p16 (n = 4), phospho-Rb/total-Rb (n = 4) and PCNA (n = 3) from (a). Data presented as means ± s.e.m., P values as indicated by unpaired t-test, two-tailed statistical analysis. (f) Analysis of cell numbers in human fibroblasts after 96-hour treatment with non-targeting or SIRT3 siRNA. n = 4 per group; Data presented as means ± s.e.m., P values as indicated by unpaired t-test, two-tailed statistical analysis. (g) Western blot analyses of expression levels of SIRT3, Col1a1, CTGF and Bim in human fibroblasts after treatment with non-targeting or SIRT3 siRNA. (h-k) Quantitative analysis of SIRT3, Col1a1, CTGF and Bim levels from experiment described in (g). n = 3 per group; Data presented as means ± s.e.m., P values as indicated by unpaired t-test, two-tailed statistical analysis. (l, m) IMR-90 fibroblasts transfected for 48 hours with non-targeting or SIRT3 specific siRNA were analyzed for β-galactosidase staining (Scale bar 50 μm) (l) and for caspase-3 activity (m). n = 3 per group; Data presented as means ± s.e.m., P values as indicated by unpaired t-test, two-tailed statistical analysis.