fig9

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 9. Activation of the DNA Damage Response (DDR) pathway. (A) Immunofluorescence panels showing expression of phospho-H2AFX, a marker for the double-stranded DNA breaks (DSBs) in the myocardial sections. (B) Quantitative data showing the percentage of nuclei staining positive for the expression of pH2AFX. (C) Immunofluorescence panels showing expression of phospho-H2AFX in isolated cardiac fibroblasts. Panels representing the expression of pH2AFX (green color), PDGFRA (red), and the overlay are presented along with enlarged inserts showing the expression of pH2AFX in the nuclei of isolated cardiac fibroblasts. (D) Graph depicting the percentage of the cells co-expressing PDGFRA and pH2AFX in the experimental and control groups. (E) Immunoblots showing expression of selected proteins involved in the DDR pathways, namely pH2AFX, total H2AFX, ATN, and CGAS, along with blot representing controls for the loading conditions, are shown in the WT, Pdgfra-Cre, Pdgfra-Cre:LmnaW/F, and Pdgfra-Cre:LmnaW/F mice. (F) Quantitative data corresponding to the blots shown in panel C.

The Journal of Cardiovascular Aging

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