CircRNA circCOL1A1 Acts as a Sponge of miR-30a-5p to Promote Vascular Smooth Cell Phenotype Switch through Regulation of Smad1 Expression

Author:

Ye Meng1,Ni Qihong1,Wang Han1,Wang Yuli1,Yao Yongjie1,Li Yinan1,Wang Weilun1,Yang Shuofei1,Chen Jiaquan1,Lv Lei1,Zhao Yiping1,Xue Guanhua1,Guo Xiangjiang1,Zhang Lan1ORCID

Affiliation:

1. Department of Vascular Surgery, Renji Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China

Abstract

Phenotypic switch of vascular smooth muscle cells (VSMCs) plays an important role in the pathogenesis of atherosclerosis. The mRNA expression of the synthetic biomarker Collagen Type I Alpha 1 Chain (COL1A1) gene is upregulated during the switch of VSMCs from the contractile to the synthetic phenotype. The association of noncoding circular RNAs transcribed by the COL1A1 gene with VSMC phenotype alteration and atherogenesis remains unclear. Here we reported a COL1A1 circular RNA (circCOL1A1) which is specifically expressed in VSMCs and is upregulated during phenotype alteration of VSMCs. CircCOL1A1 is also detectable in the serum or plasma. Healthy vascular tissues have a low expression of CircCOL1A1, while it is upregulated in atherosclerosis patients. Through ex vivo and in vitro assays, we found that circCOL1A1 can promote VSMC phenotype switch. Mechanistic analysis showed that circCOL1A1 may exert its function as a competing endogenous RNA of miR-30a-5p. Upregulation of circCOL1A1 ameliorates the inhibitory effect of miR-30a-5p on its target SMAD1, which leads to suppression of transforming growth factor-β (TGF-β) signaling. Our findings demonstrate that circCOL1A1 promotes the phenotype switch of VSMCs through the miR-30a-5p/SMAD1/TGF-β axis and it may serve as a novel marker of atherogenesis or as a therapeutic target for atherosclerosis.

Funder

“Star of Jiao-Tong University” Medical-Industry Interdisciplinary Research Fund

National Nature Science Foundation of China

Publisher

Georg Thieme Verlag KG

Subject

Hematology

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