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LncRNA CRNDE regulates the proliferation and migration of vascular smooth muscle cells
Author(s) -
Zhou Yu,
He Xuyu,
Liu Ruiming,
Qin Yuansen,
Wang Shenming,
Yao Xi,
Li Chunying,
Hu Zuojun
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28284
Subject(s) - vascular smooth muscle , microbiology and biotechnology , cell growth , smooth muscle , chemistry , biology , endocrinology , biochemistry
Restenosis after angioplasty or stent is a major clinical problem. While long noncoding RNAs (lncRNAs) are implicated in a variety of diseases, their role in restenosis is not well understood. This study aims to investigate how dysregulated lncRNAs and messenger RNAs (mRNAs) contribute to restenosis. By microarray analysis, we identified 202 lncRNAs and 625 mRNAs (fold change > 2.0, p < 0.05) differentially expressed between the balloon‐injured carotid artery and uninjured carotid artery in the rats. Among differentially expressed lncRNAs, LncRNA CRNDE had the highest fold change and the change was validated by reverse transcription polymerase chain reaction. We found that LncRNA CRNDE was significantly upregulated in injured rat carotid artery and vascular smooth muscle cells (VSMCs) stimulated by platelet‐derived growth factor‐BB (PDGF‐BB). Knockdown of LncRNA CRNDE by small interference RNA significantly inhibited PDGF‐BB stimulated proliferation and migration of VSMCs. Moreover, knockdown of LncRNA CRNDE attenuated PDGF‐BB‐induced phenotypic change of VSMCs. Taken together, our study reveals a novel mechanoresponsive LncRNA CRNDE which may be a therapeutic target for restenosis.