VEGF induces stress fiber formation in fibroblasts isolated from dystrophic muscle

摘要: Treatment with vascular endothelial growth factor (VEGF) to reduce ischemia and enhance both endogenous muscle repair regenerative cell therapy in Duchenne muscular dystrophy (DMD) has been widely proposed recent years. However, the interaction between angiogenesis fibrosis, a hallmark feature of DMD, remains unclear. To date, it not determined whether VEGF exerts pro-fibrotic effect on DMD-derived fibroblasts, which may contribute further disease progression. Thus, purpose this study was investigate exogenous fibroblast cultures established from murine model DMD. Primary were gastrocnemius diaphragm muscles 10 week-old mdx/utrn+/- mice. Quantitative polymerase chain reaction (qPCR) employed assess changes transcript expression alpha-smooth actin (Acta2), type-1 collagen (Col1a1), connective tissue (Ctgf/ccn2) fibronectin (Fn1). Immunofluorescence Western blot analysis visualize protein (α-SMA), CTGF/CCN2 fibronectin. mRNA levels Col1a1, Ctgf/ccn2, FN did increase following treatment fibroblasts derived either or muscles. Acta2 increased significantly diaphragm-derived VEGF. Morphological assessment revealed stress fiber formation VEGF-treated compared untreated control fibroblasts. The findings suggest that investigation into function is required prior utilization as for