The RNA binding protein hnRNPK protects against adriamycin-induced podocyte injury

Shili Zhao1,2, Junxia Feng2, Jingchun Li2

  • 1Department of Nephrology, The First Affiliated Hospital of Jinan University, Guangzhou, China.

Abstract

Insights

Heterogeneous nuclear ribonucleoprotein K (hnRNPK) protects against adriamycin-induced podocyte injury. Overexpression of hnRNPK reduced apoptosis and improved cell viability, offering a potential therapy for kidney disease.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Podocytes are crucial for glomerular filtration and preventing protein loss.
  • Podocyte injury can lead to apoptosis, kidney damage, and disease.
  • Understanding podocyte injury mechanisms is vital for developing effective therapies.

Purpose of the Study:

  • To investigate the role of heterogeneous nuclear ribonucleoprotein K (hnRNPK) in adriamycin (ADR)-induced podocyte injury.
  • To explore hnRNPK's potential as a therapeutic target for kidney disease.

Main Methods:

  • Quantitative real-time PCR and western blot to assess synaptopodin, nephrin, and hnRNPK expression.
  • Cell Counting Kit-8, EdU assay, and Hoechst 32258 staining to evaluate proliferation and apoptosis.
  • JC-1 staining, LDH assay, and ROS detection kit to measure mitochondrial function and oxidative stress.
  • HE staining for histological analysis in mouse models.

Main Results:

  • ADR treatment downregulated synaptopodin and nephrin in podocytes.
  • hnRNPK overexpression counteracted ADR's negative effects on podocyte proliferation and apoptosis.
  • ADR-induced LDH leakage and ROS generation were reduced by hnRNPK treatment.

Conclusions:

  • hnRNPK ameliorates ADR-induced podocyte injury both in vitro and in vivo.
  • hnRNPK represents a promising therapeutic strategy for preventing podocyte injury and kidney disease.

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