LncRNA Snhg8 attenuates microglial inflammation response and blood–brain barrier damage in ischemic stroke through regulating miR‐425‐5p mediated SIRT1/NF‐κB signaling. Issue 5 (25th January 2021)

• Record Type: Journal Article
• Authors: Tian, Jianan; Liu, Yihang; Wang, Zhenqi; Zhang, Siqi; Yang, Yue; Zhu, Yulan; Yang, Chunxiao
• Is Part Of: Journal of biochemical and molecular toxicology. Volume 35:Issue 5(2021)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2021-01-25
• Subjects: brain–blood barrier -- inflammation -- ischemic stroke -- microglia -- Snhg8; Biochemistry -- Periodicals; Molecular biology -- Periodicals; Toxicology -- Periodicals; 574
• DOI: 10.1002/jbt.22724
• Languages: English
• ISSNs: 1095-6670

Abstract

Abstract: Increasing studies have indicated that abnormal expressed long noncoding RNAs (lncRNAs) play a vital role in ischemic stroke. Small nucleolar RNA host gene 8 (Snhg8), a member of lncRNAs, has been found to induce neuronal apoptosis in chronic cerebral ischemia models. Here, we aim to explore the function and molecular mechanism of Snhg8 in modulating microglial inflammation as well as brain microvascular endothelial cell (BMEC) damage following ischemic injury. Our data suggested that Snhg8 was low‐expressed in the brain tissues of mice that underwent middle cerebral artery occlusion (MCAO) surgery and oxygen‐glucose deprivation (OGD)‐treated primary microglia and BMECs. Gain‐ or loss‐of function approaches found that Snhg8 upregulation not only attenuated ischemic induced inflammatory response in microglia but also relieved BMECs injury both in vitro and in vivo. Furthermore, we conducted a bioinformatics analysis to explore the underlying mechanism of Snhg8. The results indicated that Snhg8 served as a competitive endogenous RNA by sponging miR‐425‐5p, which was proved to promote microglial inflammation and BMECs injury by targeting sirtuin1 (SIRT1)‐mediated nuclear factor‐κB (NF‐κB) pathway. Overall, these results revealed that the Snhg8/miR‐425‐5p/SIRT1/NF‐κB axis plays a critical role in the regulation of cerebral ischemia‐induced microglial inflammation and brain–blood barrier damage. Abstract : This is graphical abstract.