MIR210HG Aggravates Sepsis-Induced Inflammatory Response of Proximal Tubular Epithelial Cell via the NF-κB Signaling Pathway

Shuai Deng; Bin Gu; Zheng Yu; Zhen Shen; Houwei Ren

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자료유형: 학술저널

저자정보: Shuai Deng (Department of Emergency Jiangsu Taizhou People’s Hospital China.) Bin Gu (Department of Emergency Jiangsu Taizhou People’s Hospital China.) Zheng Yu (Department of Emergency Jiangsu Taizhou People’s Hospital China.) Zhen Shen (Department of Emergency Jiangsu Taizhou People’s Hospital China.) Houwei Ren (Department of Emergency Jiangsu Taizhou People’s Hospital China.)

저널정보: 연세대학교 의과대학 Yonsei Medical Journal Yonsei Medical Journal 제62권 제5호

발행연도: 2021.1

수록면: 461 - 469 (9page)

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Purpose: Acute kidney injury (AKI) is a serious complication of sepsis and is characterized by inflammatory response. MicroRNA-210 host gene (MIR210HG) is upregulated in human proximal tubular epithelial cells under treatment of inflammatory cytokines. This study aimed to explore the role of MIR210HG in sepsis-induced AKI. Materials and Methods: Cell viability was detected by a cell counting kit 8 assay. The levels of proinflammatory cytokines weredetected by enzyme-linked immunosorbent assay kits. The protein levels of p65, IκBα, and p-IκBα were examined by western blotanalysis. The nuclear translocation of nuclear factor kappa B (NF-κB) was detected by immunofluorescence assay. The histologicalchanges of kidneys were analyzed by hematoxylin and eosin staining assay. Results: Lipopolysaccharide (LPS) treatment significantly inhibited cell viability and increased productions of proinflammatorycytokines in proximal tubular epithelial cells (HKC-8). Additionally, MIR210HG levels in HKC-8 cells were increased by LPS treatment. MIR210HG silencing inhibited the LPS-induced cell inflammatory response. MIR210HG activated the NF-κB signalingpathway by promoting the phosphorylation of IκBα and nuclear translocation of p65. Rescue assays revealed that the MIR210HGinducedincrease of cytokines levels and decline of cell viability were rescued by QNZ treatment. Knockdown of MIR210HG decreasedblood urea nitrogen, serum creatinine, and proinflammatory cytokine levels in AKI rats. Moreover, the knockdown ofMIR210HG protected against AKI-induced histological changes of kidneys in rats. Conclusion: MIR210HG promotes sepsis-induced inflammatory response of HKC-8 cells by activating the NF-κB signaling pathway. This novel discovery may be helpful for the improvement of sepsis-induced AKI.

#MIR210HG #sepsis #AKI #NF-κB signaling

참고문헌 (39)

참고문헌 신청

Poston JT / 2019 / Sepsis associated acute kidney injury / BMJ 364:k4891

Romagnoli S / 2018 / CRRT for sepsis-induced acute kidney injury / Curr Opin Crit Care 24:483~492

Zarbock A / 2014 / Sepsis-induced acute kidney injury revisited : pathophysiology, prevention and future therapies / Curr Opin Crit Care 20:588~595

Umbro I / 2016 / Recent advances in pathophysiology and biomarkers of sepsis-induced acute kidney injury / J Infect 72:131~142

Wang P / 2015 / Exogenous carbon monoxide decreases sepsis-induced acute kidney injury and inhibits NLRP3 inflammasome activation in rats / Int J Mol Sci 16:20595~20608

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