Omi inhibition ameliorates neuron apoptosis and neurological deficit after subarachnoid hemorrhage in rats

Du Yuanfeng; Yang Dingbo; Dong Xiaoqiao; Du Quan; Wang Ding; Shen Yongfeng; Yu Wenhua

doi:10.1007/s13258-021-01176-y

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자료유형: 학술저널

저자정보: Du Yuanfeng (Nanjing Medical University Affiliated Hangzhou Hospital China) Yang Dingbo (Nanjing Medical University Affiliated Hangzhou Hospital China) Dong Xiaoqiao (Nanjing Medical University Affiliated Hangzhou Hospital China) Du Quan (Nanjing Medical University Affiliated Hangzhou Hospital China) Wang Ding (Nanjing Medical University Affiliated Hangzhou Hospital China) Shen Yongfeng (Nanjing Medical University Affiliated Hangzhou Hospital China) Yu Wenhua (Nanjing Medical University Affiliated Hangzhou Hospital China)

저널정보: 한국유전학회 Genes & Genomics Genes & Genomics Vol.43 No.12

발행연도: 2021.12

수록면: 1,423 - 1,432 (10page)

DOI: 10.1007/s13258-021-01176-y

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Background Subarachnoid hemorrhage (SAH) is a severe neurological emergency, resulting in cognitive impairments and threatening human's health. Currently, SAH has no efective treatment. It is urgent to search for an efective therapy for SAH. Objective To explore the expression of Omi protein after subarachnoid hemorrhage in rats. Methods SAH rat model was established by injecting blood into the prechiasmatic cistern. Neurological defcit was assessed by detecting neurological defcit scores and brain tissue water contents. Apoptotic cells were evaluated by TUNEL staining and IHC staining. Omi and Cleaved caspase 3 expressions in nerve cells were determined by double staining using IF. Apoptosis-related proteins were measured by Western blotting assay. Results SAH rat model was successfully established, showing more apoptotic cells and high neurological defcit scores in SAH rat. In SAH rat model, Omi expression in nerve cells was elevated and the upregulation of Omi mainly occurred in cytoplasm, accompanied by the degradation of XIAP and the increased cleaved caspase 3/9 and cleaved PARP. Once treated with UCF-101, a specifc inhibitor of Omi, the increased cell apoptosis, left/right brain moisture contents and neurological defcits were notably reversed in SAH rat brain. Of note, SAH-induced the increases of apoptosis-related protein in nerve cells were also rescued by the administration of UCF-101. Conclusions UCF-101-mediated Omi inhibition decreased the degradation of XIAP and subsequently inhibited the activation of apoptosis-related proteins, decreased nerve cell apoptosis, leading to the improvement on early brain injury in SAH rat. UCF-101-based Omi inhibition may be used to treat SAH with great potential application.

#Protease Omi #Subarachnoid hemorrhage #Neurological deficit #Cell apoptosis #Early brain injury

참고문헌 (42)

참고문헌 신청

Althaus J / 2007 / The serine protease Omi/HtrA2 is involved in XIAP cleavage and in neuronal cell death following focal cerebral ischemia/reperfusion / Neurochem Int 50:172~180

Burkhardt JK / 2017 / Rapid documented growth of aneurysm bleb led to rupture of an incidental intracranial anterior communicating artery aneurysm / J Neurol Surg Part A 78:521~524

Chen S / 2014 / Controversies and evolving new mechanisms in subarachnoid hemorrhage / Prog Neurobiol 115:64~91

Yuhyun Chung / 2018 / Dysregulated autophagy contributes to caspase-dependent neuronal apoptosis / Cell Death & Disease 9(12)

Chung HJ / 2020 / Neuroprotective function of Omi to alpha-synuclein-induced neurotoxicity / Neurobiol Dis 136:104706

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