1. Fstl1 promotes cardiac fibroblasts proliferation via the ERK1/2‐dependent pathway
Fstl1 promotes cardiac fibroblasts proliferation via the ERK1/2‐dependent pathway A, BFibroblast proliferation was assessed by Edu incorporation assay. Endogenous Fstl1 was ablated by siRNA. NRCFbs were cultured in 0.5% FBS condition for 48 h to synchronize the cell cycle. EdU (10 μM as the final concentration) was added into media at 4 h before harvest. Error bars represent mean ± SEM (n = 5, each group). Statistical analysis was performed by unpaired t‐test (two‐tailed). Two independent experiments were performed. (B) Effect of exogenous Fstl1 on cardiac fibroblast proliferation. Cells were cultured in FBS 0.5% media for 24 h. Recombinant Fstl1 (50 ng/ml) or vehicle was added to 2% FBS‐containing media and cultured for 48 h. EdU was added into media at 4 h before harvest. Error bars represent mean ± SEM (n = 7, each group). Statistical analysis was performed by unpaired t‐test (two‐tailed). Two independent experiments were performed.CFstl1‐promoted fibroblast proliferation was diminished by PD PD98059 (5 nM) was added 30 min prior to recombinant Fstl1 stimulation (50 ng/ml). The cells were cultured for 48 h, and EdU was added into media at 4 h before harvest. Error bars represent mean ± SEM (n = 4–10, per treatment group). Statistical analysis was performed by one‐way ANOVA and Tukey's multiple comparison test. Two independent experiments were performed.DSchema of the role of Fstl1 in infarct repair. Fstl1 is upregulated by TGF‐β1 in infarcted heart, and it contributes to the proliferation and migration of fibroblasts into the infarcted site and border zone. These actions increase the number of myofibroblasts (MyoFB) in the infarcted lesion. In turn, fibroblasts and myofibroblasts synthesize ECM components including collagens and fibronectin and protect the infarcted heart from rupture. Source data are available online for this figure.
Sonomi Maruyama et al. EMBO Mol Med. 2016;8:
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