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

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 7. Myocardial adipocytes. (A) Thin myocardial sections were stained for the expression of perilipin 1 (PLIN1), a marker for triglyceride-rich adipocytes in 6 weeks old mice. (B) Quantitative data showing the number of cells stained positive for the expression of PLIN1 per myocardial section in the experimental and control groups at six weeks of age. (C) Transcript levels of selected markers of adipogenesis, quantified by RT-PCR, in the control and experimental groups. (D) Thin myocardial sections were stained for the expression of PLIN1 in the one-year-old Pdgfra-Cre:Lmna^W/F and the control mice. (E) Quantitative data showing the number of PLIN1 expressing cells per section in one-year-old WT, Pdgfra-Cre, and Pdgfra-Cre:Lmna^W/F mice. (F) Transcript levels of selected markers of adipogenesis in one-year-old WT, Pdgfra-Cre, and Pdgfra-Cre:Lmna^W/F mice.

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Committee on Publication Ethics

Portico

Committee on Publication Ethics

Portico