FoxC1-Induced Vascular Niche Improves Survival and Myocardial Repair of Mesenchymal Stem Cells in Infarcted Hearts
FoxC1 enhances MSC-mediated amelioration of MI pathology. (a, b) Representative high-magnification images of H&E staining (a) (yellow arrows, inflammatory cell infiltration; white arrowheads, myocyte necrosis) and Masson’s trichrome staining (b) (none of the infarcted myocardium was stained red; pale region, infarcted myocardium; bright red, viable myocardium; bright blue, fibrosis) at 30 days post-MI. . (c–h) Quantitative analysis of inflammatory cells (c), viable myocardium (d), MPO (e), ROS (f), infarct size (g), and collagen content (h) 30 days after cell therapy (45 d post-MI). All graphical data are the . vs. CON+PBS, † vs. CON+MSCs, ‡ vs. adFoxC1+PBS, § vs. adFoxC1+MSCs, and || vs. siFoxC1+PBS (CON IHs: PBS, , and MSCs, ;adFoxc1: PBS, , and MSCs, ;siFoxC1: PBS , and MSCs, ); Student’s -test. FoxC1 enhanced the reduction of myocardial inflammation and collagen and increased angiogenesis induced by MSC therapy, suggesting that FoxC1 may contribute to the amelioration of MI pathology in cooperation with MSC therapy.
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