miR-204-5p is sponged by TUG1 to aggravate neuron damage induced by focal cerebral ischemia and reperfusion injury through upregulating COX2

Pu Xiang; Jian Hu; Hong Wang; Ying Luo; Chao Gu; Xiaodan Tan; Yujun Tu; Wenjia Guo; Lin Chen; Lin Gao; Rongchun Chen; Junqing Yang

doi:10.1038/s41420-022-00885-x

miR-204-5p is sponged by TUG1 to aggravate neuron damage induced by focal cerebral ischemia and reperfusion injury through upregulating COX2

Cell Death Discov. 2022 Feb 28;8(1):89. doi: 10.1038/s41420-022-00885-x.

Authors

Pu Xiang^#^{1

2}, Jian Hu^#³, Hong Wang¹, Ying Luo¹, Chao Gu¹, Xiaodan Tan¹, Yujun Tu¹, Wenjia Guo¹, Lin Chen⁴, Lin Gao⁴, Rongchun Chen¹, Junqing Yang⁵

Affiliations

¹ Department of Pharmacology, Chongqing Medical University, the Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing, 400016, China.
² Department of Pharmacy, Dianjiang People's Hospital of Chongqing, Chongqing, 408300, China.
³ Department of Hepatobiliary Surgery, Dianjiang People's Hospital of Chongqing, Chongqing, 408300, China.
⁴ Department of Neurology, Dianjiang People's Hospital of Chongqing, Chongqing, 408300, China.
⁵ Department of Pharmacology, Chongqing Medical University, the Key Laboratory of Biochemistry and Molecular Pharmacology, Chongqing, 400016, China. cqyangjq@cqmu.edu.cn.

^# Contributed equally.

Abstract

Studies have reported that miR-204-5p is involved in multiple biological processes. However, little is known about the expression and mechanism of miR-204-5p in cerebral ischemia and reperfusion injury. This study found that miR-204-5p expression was significantly downregulated in the blood of patients with ischemic stroke, MCAO/R rat brains, and OGD/R neurons. Overexpression of miR-204-5p markedly reduced infarct volume and neurological impairment and alleviated the inflammatory response in vivo. miR-204-5p promoted neuronal viability and reduced apoptotic cells in vitro. Mechanically, miR-204-5p was negatively regulated by the expression lncRNA TUG1 upstream and down-regulated COX2 expression downstream. Therefore, the TUG1/miR-204-5p/COX2 axis was involved in ischemia and reperfusion-induced neuronal damage. This finding may provide a novel strategy for the treatment of cerebral ischemia and reperfusion injury.

Abstract

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