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HIPK2基因对缺氧复氧诱导的NRK-52E肾小管上皮细胞活力和凋亡及JAK2/STAT3信号通路的影响

朱彬蔚 卞蓉蓉 陈冬平 梅长林

中国病理生理杂志2018,Vol.34Issue(6):1075-1080,6.
中国病理生理杂志2018,Vol.34Issue(6):1075-1080,6.DOI:10.3969/j.issn.1000-4718.2018.06.019

HIPK2基因对缺氧复氧诱导的NRK-52E肾小管上皮细胞活力和凋亡及JAK2/STAT3信号通路的影响

Effect of HIPK2 gene on viability, apoptosis and JAK2/STAT3 signaling pathway in NRK-52E renal tubular epithelial cells induced by hypoxia and reoxygenation

朱彬蔚 1卞蓉蓉 1陈冬平 1梅长林1

作者信息

  • 1. 第二军医大学长征医院肾内科,上海200001
  • 折叠

摘要

Abstract

AIM:To investigate the effect of homeodomain-interacting protein kinase 2 (HIPK2) on the viabi-lity, apoptosis and JAK2/STAT3 signaling pathway in NRK-52E renal tubular epithelial cells induced by hypoxia and reox-ygenation (H/R). METHODS:HIPK2 small interfering RNA (siRNA) was transfected into NRK-52E cells by Lipo-fectamineTM 2000, and normal control group (control group) and negative control group (HIPK2-NC group) were set up. After H/R, the cell viability was measured by CCK-8 assay, the apoptotic rate and Ca2+ fluorescence intensity were ana-lyzed by flow cytometry, and the protein levels of Ki67, cleaved caspase-3, caspase-12, Bcl-2, Bax, p-JAK2 and p-STAT3 were determined by Western blot. RESULTS:Compared with control group, the protein expression of HIPK2 in the NRK-52E cells was significantly decreased after transfection with HIPK2 siRNA (P<0.05). Compared with control group, the cell viability and the protein expression of Ki67 and Bcl-2 in H/R group were also significantly decreased, and the apoptotic rate, the Ca2+ fluorescence intensity and the protein levels of cleaved caspase-3, caspase-12, Bax, p-JAK2 and p-STAT3 were significantly increased (P<0.05). Compared with H/R group, the cell viability and the protein expression of Ki67 and Bcl-2 in HIPK2-siRNA+H/R group were significantly increased, while the apoptotic rate, the Ca2+ fluorescence inten-sity and the protein levels of cleaved caspase-3, caspase-12, Bax, p-JAK2 and p-STAT3 were significantly decreased (P<0.05). CONCLUSION:Inhibition of HIPK2 gene expression promotes H/R-induced growth of NRK-52E renal tubular epi-thelial cells, and reduces the apoptosis. The mechanism is related to down-regulating the JAK2/STAT3 signaling pathway.

关键词

HIPK2基因/肾小管上皮细胞/缺氧/复氧/细胞凋亡/JAK2/STAT3信号通路

Key words

HIPK2 gene/Renal tubular epithelial cells/Hypoxia/Reoxygenation/Apoptosis/JAK2/STAT3 signaling pathway

分类

医药卫生

引用本文复制引用

朱彬蔚,卞蓉蓉,陈冬平,梅长林..HIPK2基因对缺氧复氧诱导的NRK-52E肾小管上皮细胞活力和凋亡及JAK2/STAT3信号通路的影响[J].中国病理生理杂志,2018,34(6):1075-1080,6.

基金项目

国家自然科学基金青年科学基金资助项目(No.8140041470) (No.8140041470)

中国病理生理杂志

OA北大核心CSCDCSTPCD

1000-4718

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