miR-204-5p is sponged by TUG1 to aggravate neuron damage induced by focal cerebral ischemia and reperfusion injury through upregulating COX2.
Pu XiangJian HuHong WangYing LuoChao GuXiaodan TanYujun TuWenjia GuoLin ChenLin GaoRongchun ChenJunqing YangPublished in: Cell death discovery (2022)
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.
Keyphrases
- cerebral ischemia
- subarachnoid hemorrhage
- blood brain barrier
- brain injury
- poor prognosis
- inflammatory response
- oxidative stress
- binding protein
- transcription factor
- acute myocardial infarction
- spinal cord
- acute coronary syndrome
- left ventricular
- signaling pathway
- diabetic rats
- long noncoding rna
- percutaneous coronary intervention
- lps induced
- pi k akt
- replacement therapy