1. Long noncoding RNA SNHG1 protects brain microvascular endothelial cells against oxygen–glucose deprivation/reoxygenation-induced injury by sponging miR-298 and upregulating SIK1 expression
- Author
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Xinyu Zhou, Bingchao Xu, Niu Ji, Yan Gu, Pin Meng, and Lingdan Dong
- Subjects
0106 biological sciences ,0301 basic medicine ,Cell Survival ,Bioengineering ,Protein Serine-Threonine Kinases ,Models, Biological ,01 natural sciences ,Applied Microbiology and Biotechnology ,Cell Line ,Mice ,03 medical and health sciences ,Downregulation and upregulation ,010608 biotechnology ,Animals ,Small nucleolar RNA ,Cell Proliferation ,Ischemic Stroke ,Gene knockdown ,Cell growth ,Chemistry ,Kinase ,Brain ,Endothelial Cells ,General Medicine ,Long non-coding RNA ,Up-Regulation ,Cell biology ,MicroRNAs ,030104 developmental biology ,Gene Expression Regulation ,Apoptosis ,Gene Knockdown Techniques ,RNA, Long Noncoding ,Function (biology) ,Biotechnology - Abstract
Growing evidence shows that long non-coding RNAs (lncRNAs) are widely involved in the progression of multiple diseases, including ischemic stroke. The aim of this study was to explore the function and underlying mechanism of lncRNAs small nucleolar RNA host gene 1 (SNHG1) in ischemic stroke. SNHG1 and salt-induced kinase 1 (SIK1) were upregulated in oxygen–glucose deprivation/reperfusion (OGD/R)-induced bEnd3 cells. SNHG1 downregulation promoted OGD/R-induced injury through decreasing cell proliferation and increasing apoptosis, which was reversed by upregulating SIK1 or downregulating miR-298. Moreover, SIK1 interference had similar functions with SNHG1 knockdown in OGD/R-treated bEnd3 cells. In addition, miR-298 was a direct target of SNHG1 and could specifically bind to SIK1. Furthermore, SNHG1 functioned as a molecular sponge of miR-298 to regulate SIK1 expression. SNHG1 knockdown enhanced OGD/R-induced injury in bEnd3 cells by regulating miR-298/SIK1 axis, which might provide promising therapeutic target for treatment of ischemic stroke.
- Published
- 2021