fig10

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 10. Expression of senescence markers. (A) Immunoblots showing levels of phospho-TP53 S18 and S389 proteins as well as the bonafide downstream target of activation of TP53, namely CDKN1A, in the experimental groups. (B) Quantitative data representing the blots shown in panel A. (C) Thin myocardial sections were stained for the expression of senescence-associated β-galactosidase, detecting its expression in the heart of 6-week-old Pdgfra-Cre:LmnaF/F mice. (D) Immunoblots showing increased expression levels of CTGF (CCN2) and LGALS3, SASP markers, in the Pdgfra-Cre:LmnaF/F mouse hearts. Quantitative data are shown in panels (E and F). (G) Transcript levels of selected senescence-associated secretory phenotype (SASP), quantified by RT-PCR, showing increased transcript levels in the Pdgfra-Cre:LmnaF/F mouse hearts, as compared to other genotypes.

The Journal of Cardiovascular Aging

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