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. Author manuscript; available in PMC: 2020 Jun 4.
Published in final edited form as: Cell Metab. 2019 Mar 28;29(6):1274–1290.e9. doi: 10.1016/j.cmet.2019.03.001

Fig. 7. NMN-dependent rescue of fibrosis, telomere maintenance, suppression of DNA damage response and improvement of mitochondrial function is partially Sirt1 dependent.

Fig. 7

(a-c) Sirt1 deficiency in G4 mice significantly abrogates the beneficial effect of NMN in TAA-induced fibrosis in G4 mice as determined by (a) Sirius red staining, (b) hydroxyproline quantification and (c) fibrosis score (8 mice per group; p <0.05); (d) NMN-induced telomere length in G4 is partially Sirt1 dependent as shown by decreased telomere signal in the absence of Sirt1 in G4 mice treated with TAA; WT and Sirt1 deficient mice do not show discernable differences in telomere length with NMN; right graph shows quantification of telomere length (8 mice per group were analyzed; between 560-640 nuclei were quantified per group); (e, f) NMN-induced repression of p53 and p53 targets in G4 mice is largely Sirt1 dependent as indicated by (e) similar p53 protein levels in G4/Sirt -/mice treated with NMN compared to untreated G4/Sirt −/− untreated controls and (f) increased p53 targets (p21, Bax and Gadd45a, f) in G4/Sirt1 −/− ( 8 mice per group were analyzed); NMN-induced expression of (g) mitochondrial biogenesis factors Pgc-1α, Pgc-1β, Errα and Tfam, (h) mtDNA copy number and (i) complex I and IV activity mice is partially Sirt1 dependent in G4 mice (8 mice per group analyzed); Results are expressed as mean ± s.e.m.; t-test was used to determine statistical significance with p <0.05 considered as significant, as indicated by (*).