Inhibition of Long Noncoding RNA SNHG15 Ameliorates Hypoxia/Ischemia-Induced Neuronal Damage by Regulating miR-302a-3p/STAT1/NF-κB Axis

Guogang Luo; Chunting Hu; Chen Li; Qiaoya Ma; Ruili Wang; Ya He; Hui Wang

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자료유형: 학술저널

저자정보: Guogang Luo (The First Affiliated Hospital of Xi’an Jiaotong University China) Chunting Hu (The Second Affiliated Hospital of Xi’an Jiaotong University China) Chen Li (The Second Affiliated Hospital of Xi’an Jiaotong University China) Qiaoya Ma (The Second Affiliated Hospital of Xi’an Jiaotong University China) Ruili Wang (The Second Affiliated Hospital of Xi’an Jiaotong University China) Ya He (The Second Affiliated Hospital of Xi’an Jiaotong University China) Hui Wang (The Second Affiliated Hospital of Xi’an Jiaotong University China)

저널정보: 연세대학교 의과대학 Yonsei Medical Journal Yonsei Medical Journal 제62권 제4호

발행연도: 2021.1

수록면: 325 - 337 (13page)

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Purpose: Ischemic brain injury results in high mortality and serious neurologic morbidity. Here, we explored the role of SNHG15in modulating neuronal damage and microglial inflammation after ischemia stroke. Materials and Methods: The hypoxia/ischemia models were induced by middle cerebral artery occlusion in mice and oxygenglucosedeprivation/reoxygenation (OGD/R) in vitro. Quantitative real-time PCR (qRT-PCR) and Western blot were conducted todetermine the levels of SNHG15, miR-302a-3p, and STAT1/NF-κB. Moreover, gain- or loss-of functional assays of SNHG15 and miR-302a-3p were conducted. MTT assay was used to evaluate the viability of HT22 cells, and the apoptotic level was determined byflow cytometry. Furthermore, enzyme-linked immunosorbent assay was performed to detect oxidative stress and inflammatorymediators in the ischemia cortex and OGD/R-treated BV2 microglia. Results: The SNHG15 and STAT1/NF-κB pathways were both distinctly up-regulated, while miR-302a-3p was notably down-regulatedin the ischemia cortex. Additionally, overexpressing SNHG15 dramatically enhanced OGD/R-mediated neuronal apoptosisas well as the expression of oxidative stress and inflammation factors from microglia. In contrast, knocking down SNHG15 or overexpressingmiR-302a-3p relieved OGD/R-mediated neuronal apoptosis and microglial activation. Moreover, the rescue experimenttestified that overexpressing miR-302a-3p also attenuated SNHG15 up-regulation-induced effects. In terms of the mechanisms,SNHG15 sponged miR-302a-3p and activated STAT1/NF-κB as a competitive endogenous RNA, while miR-302a-3p targetedSTAT1 and negatively regulated the STAT1/NF-κB pathway. Conclusion: SNHG15 was up-regulated in the hypoxia/ischemia mouse or cell model. The inhibition of SNHG15 ameliorates ischemia/hypoxia-induced neuronal damage and microglial inflammation by regulating the miR-302a-3p/STAT1/NF-κB pathway.

#Ischemic stroke #small nucleolar RNA host gene 15 #miR-302a-3p #STAT1 #inflammation

참고문헌 (37)

참고문헌 신청

Ren C / 2020 / Ligustilide provides neuroprotection by promoting angiogenesis after cerebral ischemia / Neurol Res 42:683~692

Li B / 2017 / Brain-immune interactions in perinatal hypoxic-ischemic brain injury / Prog Neurobiol 159:50~68

Tobin MK / 2014 / Neurogenesis and inflammation after ischemic stroke : what is known and where we go from here / J Cereb Blood Flow Metab 34:1573~1584

Yu W / 2018 / Propofol prevents oxidative stress by decreasing the ischemic accumulation of succinate in focal cerebral ischemia-reperfusion injury / Neurochem Res 43:420~429

Shan W / 2020 / Long noncoding RNA TUG1 contributes to cerebral ischaemia/reperfusion injury by sponging mir-145 to up-regulate AQP4 expression / J Cell Mol Med 24:250~259

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Guogang Luo

소속기관 Xi'an Jiaotong University, Xi'an, China

주요연구분야 의약학 > 의학 일반

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Chunting Hu