Oncotarget

Research Papers:

MiR-26a contributes to the PDGF-BB-induced phenotypic switch of vascular smooth muscle cells by suppressing Smad1

Xiaoyan Yang, Mei Dong, Hao Wen, Xiaoling Liu, Meng Zhang, Lianyue Ma, Cheng Zhang, Xiaorong Luan, Huixia Lu and Yun Zhang _

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Oncotarget. 2017; 8:75844-75853. https://doi.org/10.18632/oncotarget.17998

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Abstract

Xiaoyan Yang1,2,*, Mei Dong1,*, Hao Wen1, Xiaoling Liu1, Meng Zhang1, Lianyue Ma1, Cheng Zhang1, Xiaorong Luan1, Huixia Lu1 and Yun Zhang1

1The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Department of Cardiology, Shandong University Qilu Hospital, Jinan, Shandong, China

2Department of Cardiology, Beijing Chaoyang Hospital, Capital Medical University, Beijing, China

*These authors contributed equally to this work

Correspondence to:

Yun Zhang, email: [email protected]

Huixia Lu, email: [email protected]

Keywords: miR-26a, vascular smooth muscle cells, PDGF-BB, phenotype, vascular disease

Received: September 24, 2015     Accepted: May 06, 2017     Published: May 18, 2017

ABSTRACT

The phenotypic switch of vascular smooth muscle cells (VSMCs) is a key event in the pathogenesis of various vascular diseases, such as atherosclerosis and post-angioplasty restenosis. Small non-coding microRNAs (miRNAs) have emerged as critical modulators of VSMC function. In the present study, miR-26a was significantly increased in cultured VSMCs stimulated by platelet-derived growth factor-BB (PDGF-BB) and in arteries with neointimal lesion formation. Moreover, we demonstrated that miR-26a regulates the expression of VSMC differentiation marker genes such as α-smooth muscle actin (α-SMA), calponin and smooth muscle myosin heavy chain (SM-MHC) in PDGF-BB-treated VSMCs. We further confirmed that the regulatory effect of miR-26a during the phenotypic transition occurs through its target gene Smad1, which is a critical mediator of the pro-contractile signal transmitted by bone morphogenetic protein (BMP) and transforming growth factor-beta (TGF-β). This discovery proposed a new channel for communication between PDGF and the BMP/TGF-β family. We concluded that miR-26a is an important regulator in the PDGF-BB-mediated VSMC phenotypic transition by targeting Smad1. Interventions aimed at miR-26a may be promising in treating numerous proliferative vascular disorders.


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PII: 17998