LncRNA MALAT1 regulates smooth muscle cell phenotype switch via activation of autophagy
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Tie-Feng Song1,*, Li-Wen Huang1,*, Ying Yuan1, Hui-qin Wang1, Hong-Peng He1, Wen-Jian Ma1, Li-Hong Huo1, Hao Zhou1, Nan Wang1 and Tong-Cun Zhang1,2
1Key Laboratory of Industrial Fermentation Microbiology, Ministry of Education and Tianjin, College of Biotechnology, Tianjin University of Science and Technology, Tianjin 300457, P.R. China
2Institute of Biology and Medicine, Wuhan University of Science and Technology, Wuhan 430000, P.R. China
*These authors contributed equally to this work
Tong-Cun Zhang, email: [email protected]
Nan Wang, email: [email protected]
Keywords: vascular smooth muscle cells; MALAT1; phenotype switching; autophagy; miR142-3p
Received: August 20, 2017 Accepted: November 14, 2017 Published: December 14, 2017
Vascular smooth muscle cells (VSMCs), switching from a differentiated to a proliferative phenotype, contribute to various vascular diseases. However, the role of long noncoding RNA metastasis-associated lung adenocarcinoma transcript 1 MALAT1 in the phenotype switching of VSMCs remains unclear. Here, we report that the knockdown of MALAT1 promotes the transformation of smooth muscle cells from a proliferative phenotype to a differentiated phenotype. MALAT1 knockdown inhibited cellular proliferation and migration, leading to significant cell cycle arrest in the G2 phase. MALAT1 was downregulated in bone morphogenetic protein-7 (BMP-7)-induced cellular differentiation, while MALAT1 was upregulated in platelet-derived growth factor-BB (PDGF-BB)-induced cellular proliferation. PDGF induced the transformation of smooth muscle cells into a proliferative phenotype accompanied by an increase in autophagy. The downregulation of MALAT1 attenuated PDGF-BB-induced proliferation and migration by inhibiting autophagy. MALAT1 could act as a competing endogenous RNA (ceRNA) to regulate autophagy-related 7 (ATG7) gene expression by sponging miR142-3p. The present study reveals a novel mechanism by which MALAT1 promotes the transformation of smooth muscle cells from contraction to synthetic phenotypes.
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