Skip to main content
. Author manuscript; available in PMC: 2019 Jun 3.
Published in final edited form as: Circ Res. 2016 Sep 20;119(10):1076–1088. doi: 10.1161/CIRCRESAHA.116.308895

Figure 8. Suppression of p21 expression inhibits the promotional effect of SIRT1 (Sirtuin 1) reduction on angiotensin II (Ang II)–increased vascular smooth muscle cell (VSMC) senescence and transcriptional activation of monocyte chemoattractant protein-1 (MCP-1/CCL2).

Figure 8.

A, Senescence was evaluated through the senescence-associated β-galactosidase (SA-β-gal) staining of saline or Ang Il–treated wild-type (WT) and SIRT1-VSMC–specific knockout (SV-KO) VSMCs infected with Ad-U6 (a control RNAi vector) or Ad-p21 RNAi (vectors for adenovirus-mediated knockdown of p21) for 24 h. Blue-stained cells were considered senescent. The bar represents 150 μm. B, Statistical analysis of the percentage of sA-β-gal–positive cells. Five random fields of view were analyzed for 1 group (n=7–10). C, Relative MCP-1/CCL2 mRNA expression level detected by real-time polymerase chain reaction in saline or Ang Il–treated WT and SV-KO VSMCs infected with Ad-U6 or Ad-p21 RNAi. D–F, Relative binding level of RelA/p65 to input on indicated region of human MCP-1/CCL2 promoter. *P<0.05, **P<0.01, ***P<0.001.