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Teniposide Regulates the Phenotype Switching of Vascular Smooth Muscle Cells in a miR-21-dependent Manner

Teniposide Regulates the Phenotype Switching of Vascular Smooth Muscle Cells in a miR-21-dependent Manner

Hao Han, Shu Yang, Yu Liang, Peng Zeng, Lipei Liu, Xiaoxiao Yang, Yajun Duan, Jihong Han, Yuanli Chen

Biochem Biophys Res Commun. 2018 Dec 2;506(4):1040-1046.

PMID: 30409428

Abstract:

The switch of vascular smooth muscle cells (SMCs) from the contractile phenotype to proliferative one can make contributions to atherosclerosis and neointima formation. MiR-21 can prevent the rupture of advanced lesion plaques. We previously reported the protection of DNA topoisomerase II (Topo II) inhibitors against atherosclerosis and vascular calcification. However, it remains unknown if Topo II inhibitors can change SMC phenotypes. Herein, we show that teniposide protected SMC phenotype switching during atherosclerosis by enhancing expression of smooth muscle α-actin (SMA) while reducing osteopontin (OPN) expression in aortic lesion plaques. In vitro, teniposide induced expression of smooth muscle protein 22-α and calponin 1, but inhibited expression of OPN and epiregulin in human aortic SMCs (HASMCs). Moreover, teniposide attenuated platelet derived growth factor-BB-induced HASMC proliferation and migration. Mechanistically, the effect of teniposide on SMC phenotypes was completed, at least in part, by activating miR-21 expression. In addition, teniposide ameliorated ligation-induced carotid artery remodeling in C57BL/6J mice by regulating SMA and OPN expression. Taken together, our study demonstrates that teniposide regulates SMC phenotype switching by upregulating expression of contractile genes in a miR-21-dependent manner, and this function is an important anti-atherogenic mechanism of teniposide.

Chemicals Related in the Paper:

Catalog Number	Product Name	Structure	CAS Number	Price
AP29767202	Teniposide		29767-20-2	Price

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