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Effects of homeodomain-interacting protein kinase 2 on renal tubular epithelial cells

D-L Cai1, L-X Chen, L-M Wang

  • 1Department of Geratology, The First Affiliated Hospital of Jiamusi University, Jiamusi, China. 342679500@qq.com.

European Review for Medical and Pharmacological Sciences
|June 24, 2020
PubMed
Abstract

Insights

Inhibiting homeodomain-interacting protein kinase 2 (HIPK2) reduces oxidative stress and apoptosis in kidney cells following hypoxia/reoxygenation. This protective effect is mediated via the JAK2/STAT3 signaling pathway.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Renal Physiology

Background:

  • Hypoxia/reoxygenation (H/R) induces oxidative stress (OS) and apoptosis in normal rat kidney-52E (NRK-52E) cells.
  • The role of homeodomain-interacting protein kinase 2 (HIPK2) in this process requires further investigation.

Purpose of the Study:

  • To investigate the effect of HIPK2 on OS and apoptosis in NRK-52E cells subjected to H/R.
  • To elucidate the involvement of the JAK2/STAT3 signaling pathway in HIPK2-mediated cellular responses to H/R.

Main Methods:

  • NRK-52E cells were transfected with HIPK2 small interfering RNA (siRNA).
  • Transfection efficiency was confirmed using Real Time-Polymerase Chain Reaction (RT-PCR) and Western blot (WB).
  • Cell apoptosis and OS were assessed using Cell Counting Kit-8 (CCK-8) assay, flow cytometry, TUNEL staining, PCR, and WB after H/R treatment.

Main Results:

  • siRNA-mediated inhibition of HIPK2 significantly decreased HIPK2 protein expression.
  • H/R treatment markedly increased cell apoptosis and OS in NRK-52E cells.
  • Inhibition of HIPK2 in HIPK2-siRNA + H/R group significantly reduced apoptosis and OS compared to the H/R group.

Conclusions:

  • Inhibition of HIPK2 expression promotes proliferation of NRK-52E cells under H/R conditions.
  • Downregulation of HIPK2 alleviates oxidative stress and reduces apoptosis.
  • The JAK2/STAT3 signaling pathway is implicated in the protective effects of HIPK2 inhibition against H/R-induced cellular damage.

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