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. 2018 Feb 2;8(4):1180–1194. doi: 10.7150/thno.20846

Figure 3.

Figure 3

PFL acted as a ceRNA for let-7d to promote cardiac fibrosis. (A) Decreased expression of the let-7 family in the infarcted heart. (B) Decreased expression of let-7d in the peri-infarct area at varying time points, as evaluated by qRT-PCR; GAPDH served as an internal control. (C) qRT-PCR analysis revealed that forced expression of PFL (1 μg/mL) in CFs increased mRNA expression levels of collagen 1α1 and collagen 3α1, which were reversed by let-7d overexpression; GAPDH mRNA served as an internal control. MTT assay (D) and EdU staining (E) for the assessment of cell viability and proliferation in CFs overexpressing PFL in the presence or absence of let-7d mimics. (F) Immunostaining of α-SMA in CFs demonstrated that enhanced expression of PFL promoted the fibroblast-myofibroblast transition. *p<0.05 and **p<0.01 vs. Sham mice or pcDNA3.1; #p<0.05 and ##p<0.01 vs. PFL.