fig5

Deletion of the <i>Lmna </i>gene in fibroblasts causes senescence-associated dilated cardiomyopathy by activating the double-stranded DNA damage response and induction of senescence-associated secretory phenotype

Figure 5. Myocardial fibrosis. (A) Representative images of Low (upper) and high (lower) magnification of thin myocardial sections stained for picrosirius red, which illustrates increased myocardial fibrosis in the Pdgfra-Cre:LmnaF/F mice at six weeks of age. (B) Quantitative data showing collagen volume fraction (CVF) in the experimental and control groups. (C) Immunoblot showing levels of latent and mature TGFβ1 in the control and experimental groups, which were markedly increased in the Pdgfra-Cre:LmnaW/F and Pdgfra-Cre:LmnaF/F mice. (D) Quantitative data representing the blot in panel C. (E) Transcript levels of selected markers of myocardial fibrosis, quantified by RT-PCR, in the control and experimental groups. (F) Thin myocardial sections stained for picrosirius red in the Pdgfra-Cre:LmnaW/F and control mice, showing increased myocardial fibrosis. (G) Quantitative data showing increased CVF in the Pdgfra-Cre:LmnaW/F mouse myocardium as compared to the WT and Pdgfra-Cre mice at one year of age. (H) Transcript levels of selected markers of fibrosis, showing increased levels of selected markers but not Tgfb1 in the myocardium of one-year-old Pdgfra-Cre:LmnaW/F mice.

The Journal of Cardiovascular Aging

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