KCNQ1OT1 promotes autophagy by regulating miR‐200a/FOXO3/ATG7 pathway in cerebral ischemic stroke. Issue 3 (3rd April 2019)

• Record Type: Journal Article
• Authors: Yu, Shijia; Yu, Mingjun; He, Xin; Wen, Lulu; Bu, Zhongqi; Feng, Juan
• Is Part Of: Aging cell. Volume 18:Issue 3(2019)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2019-04-03
• Subjects: ATG7 -- autophagy -- FOXO3 -- lncRNA KCNQ1OT1 -- miR‐200a -- stroke; Cells -- Aging -- Periodicals; 571.8783605
• DOI: 10.1111/acel.12940
• Languages: English
• ISSNs: 1474-9718

Abstract

Abstract: Dysregulation of long noncoding RNAs (lncRNAs) is associated with abnormal development and pathophysiology in the brain. Increasing evidence has indicated that ischemic stroke is becoming the most common cerebral disease in aging populations. The treatment of ischemic stroke is challenging, due in part to ischemia and reperfusion (I/R) injury. In this study, we revealed that potassium voltage‐gated channel subfamily Q member 1 opposite strand 1 (KCNQ1OT1) was significantly upregulated in ischemic stroke. Knockdown of KCNQ1OT1 remarkably reduced the infarct volume and neurological impairments in transient middle cerebral artery occlusion (tMCAO) mice. Mechanistically, KCNQ1OT1 acted as a competing endogenous RNA of miR‐200a to regulate downstream forkhead box O3 (FOXO3) expression, which is a transcriptional regulator of ATG7. Knockdown of KCNQ1OT1 might inhibit I/R‐induced autophagy and increase cell viability via the miR‐200a/FOXO3/ATG7 pathway. This finding offers a potential novel strategy for ischemic stroke therapy.