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. 2018 Sep 22;17(6):e12838. doi: 10.1111/acel.12838

Figure 6.

Figure 6

Telomere dysfunction causes myofibroblast transdifferentiation in a p53‐dependent manner. (a) ChIP‐qPCR analysis of p53 binding to a control distal promoter element (distal), to the αSMA promoter element (αSMA), or the p21 promoter element (p21) of normal BJ fibroblasts that were either control treated (C), treated with TGF‐β1 (10 ng/ml) for 48 hr, or transduced with shRNA targeting TRF2. Error bars: ±SD. *p < 0.05, (n = 3). (b) p53 immunoblot of BJ fibroblast cell extracts in which expression of p53 had been knocked down using two distinct shRNAs (#1 and #2). EV: knockdown using control empty vector. (c) Representative micrographs of untreated control knockdown cultures (EV; left) and TGF‐β1 treated (10 ng/ml; 48 hr) cultures in which p53 had been knocked down using shRNA (p53kd; right) or control (EV; center) that were immunostained using antibodies against α‐SMA (green) and 53PB1 (red). Nuclear DNA was counterstained with DAPI (blue). Scale bars: 20 m. (d) α‐SMA immunoblot of BJ fibroblast whole cell extracts expressing two distinct shRNAs targeting p53 (#1–2) or empty vector control (EV) that were either control treated (−) or treated with TGF‐β1 for 48 hr (+). γ‐tubulin was used as loading control. Bar graph: fold differences in α‐SMA expression levels quantified from immunoblots. ±SD. *p < 0.05, (n = 3)