LncRNA LINC01605 Regulates Smooth Muscle Cell Functions and Participates in the Development of Aortic Dissection Through Regulating SGK1
Mingliang Li, Ruonan Li, Zihe Zheng, Changbo Xiao, Quanlin Yang, Bo Chen, Xiaofu Dai
TL;DR
This study shows that the lncRNA LINC01605 promotes aortic dissection by regulating smooth muscle cell functions through SGK1.
Contribution
The novel contribution is identifying LINC01605 as a regulator of aortic dissection via its interaction with SGK1 in vascular smooth muscle cells.
Findings
LINC01605 is upregulated in aortic dissection tissues and vascular smooth muscle cells.
LINC01605 promotes VSMC proliferation, migration, and autophagy, especially under Ang II stimulation.
LINC01605 targets SGK1 and its knockdown alleviates aortic dissection pathology in mice.
Abstract
Long noncoding RNAs (lncRNAs) are emerging as key regulators in cardiovascular diseases. This study investigated the role of lncRNA LINC01605 in aortic dissection (AD) pathogenesis through its effects on vascular smooth muscle cells (VSMCs). Bioinformatics analysis of GEO datasets (GSE107844, GSE147026) identified LINC01605 as differentially expressed in AD. Its expression was validated in human aortic tissues and VSMCs using RT‐qPCR and FISH. Functional assays (CCK‐8, Transwell, Western blot) assessed VSMC proliferation, migration, phenotypic switching and autophagy. SGK1 was predicted as a target via bioinformatics and confirmed by RIP assays. Ang II‐induced AD mice with LINC01605 knockdown were used for in vivo validation. LINC01605 was significantly upregulated in AD aortic tissues and VSMCs. Functional studies demonstrated that LINC01605 promoted VSMC proliferation, migration,…
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Taxonomy
TopicsCancer-related molecular mechanisms research · Autophagy in Disease and Therapy · Congenital heart defects research