BMP-2 enhances the migration and proliferation of hypoxia-induced VSMCs via actin cytoskeleton, CD44 and matrix metalloproteinase linkage

Experimental Cell Research
Min YangWei Zhao

Abstract

The persistent proliferation of hypoxia-induced vascular smooth muscle cells (VSMCs) in the arterial wall underlie the development of atherosclerosis. However, the mechanism that regulates the behavior of VSMCs, which involve in actin aggregation, and impedes their migration is still elusive. Here, we report that bone morphogenetic protein 2 (BMP-2) leads to enrichment of CD44 and F-actin stress fiber and secretion of matrix metalloproteinases-2 (MMP-2) during hypoxia in vitro and following artificial hypoxia-induced atherosclerosis exacerbation in vivo. To test this hypothesis, fluorescence immunostaining, immune-hybridization and flow cytometry analyses were performed to understand the relationship among BMP-2, CD44 and MMP-2 linkage. The cellular actin cytoskeleton was reduced, and smaller adhesion plaques were formed in hypoxia-induced T/G HA-VSMC cell line, but BMP-2 against disruption of F-actin and increase the motility and migration behaviors of VSMC during hypoxic cultured. Aggregation of F-actin dependents on the interaction between the cell surface integral membrane protein CD44 and Vinculin which enhanced by rBMP-2. This activity of Actin/CD44/ linkage was inhibited by competing with the active site of the CD44 usin...Continue Reading

Citations

Aug 15, 2019·Experimental and Therapeutic Medicine·Zongxiang ChenJuan Du
Jun 5, 2019·Scientific Reports·Andre P MarshallRaul J Guzman
Jul 22, 2020·Clinical Chemistry and Laboratory Medicine : CCLM·Chang-Meng WuYan-Wei Hu
Jan 25, 2019·ACS Applied Materials & Interfaces·Bingcheng YiYanzhong Zhang
Sep 2, 2021·Chinese Neurosurgical Journal·Haishuang TangQiao Zuo

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