fig2

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 2. Fortuitous deletion of the Lmna gene in a subset of cardiac myocytes. (A) Immunoblots showing LMNA protein levels in cardiac myocytes isolated the WT, Pdgfra-Cre, Pdgfra-Cre:LmnaW/F, and Pdgfra-Cre:LmnaF/F mice. As in Figure 1, blots representing TNNT2 and VIM are included to assess the fidelity of the cell isolation. Blots representing GAPDH are included as controls for the loading conditions. (B) Quantitative data corresponding to the blots shown in F, showing about 30% reduction in the LMNA protein levels in the cardiac myocytes isolated from the Pdgfra-Cre:LmnaF/F mice, whereas the LMNA levels were unchanged in the myocytes isolated from the Pdgfra-Cre and Pdgfra-Cre:LmnaW/F mice. (C) Immunofluorescence staining of isolated cardiac myocytes for the PCM1 expression (upper panel), which tags cardiac myocyte nuclei in the heart, LMNA (middle panel), and the overlay (lower panel). (D) Quantitative data showing the percentages of cardiac myocytes, identified by the expression of PCM1, also express the LMNA proteins.

The Journal of Cardiovascular Aging

Portico

All published articles are preserved here permanently:

https://www.portico.org/publishers/oae/

Portico

All published articles are preserved here permanently:

https://www.portico.org/publishers/oae/