fig1

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 1. Fidelity of conditional deletion of the Lmna gene in cardiac fibroblasts. (A) Immunoblots showing LMNA protein levels in cardiac fibroblasts isolated from the wild type (WT), Pdgfra-Cre, Pdgfra-Cre:LmnaW/F, and Pdgfra-Cre:LmnaF/F mice. The upper panel shows the LMNA protein. Blots representing cardiac troponin T (TNNT2) and vimentin (VIM), as markers of cardiac myocytes and fibroblasts, are included to assess the fidelity of the cell isolation. Blots representing GAPDH are included as loading controls. (B) Quantitative data on the LMNA protein levels corresponding to the blots in panel A. (C) Immunofluorescence staining of isolated cardiac fibroblasts for the expression of PDGFRA (upper panels) and LMNA (middle panel) and the overlay (lower panel). (D) Panel D the percentages of the isolated non-myocyte cells expressing PDGFRA. (E) Percentage of the PDGFRA expressing cells in which the LMNA protein was absent. In all analyses in the present and subsequent Figures, pairwise P-values were presented only when the P-value by the one-way ANOVA test was significant.

The Journal of Cardiovascular Aging

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