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Protective effect of silencing Stat1 on high glucose-induced podocytes injury via Forkhead transcription factor

Hongkun Wang1, Yanhui Zhang1, Fangfang Xia2

  • 1Department of Nephrology, The First Affiliated Hospital of Baotou Medical College Inner Mongolia University of Science and Technology, Baotou, China.

BMC Molecular and Cell Biology
|July 25, 2019
PubMed
Abstract

Insights

Silencing Signal Transducer and Activator of Transcription 1 (Stat1) protects podocytes from high glucose injury by reducing apoptosis and oxidative stress, potentially through Forkhead box protein O1 (FoxO1) signaling.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Cell Biology

Background:

  • Podocytes are crucial for glomerular filtration barrier integrity.
  • Forkhead transcription factor O1 (FoxO1) is implicated in antioxidant signaling.
  • The role of Signal Transducer and Activator of Transcription 1 (Stat1) in high glucose-induced podocyte injury requires investigation.

Purpose of the Study:

  • To investigate the role of Stat1 in high glucose-induced podocyte injury.
  • To determine if Stat1 modulation can protect podocytes against high glucose damage.
  • To explore the relationship between Stat1 and FoxO1 in podocyte oxidative stress.

Main Methods:

  • Podocyte viability, apoptosis, and reactive oxygen species (ROS) were assessed under normal and high glucose conditions using CCK-8, flow cytometry, western blot, and qRT-PCR.
  • Stat1 was silenced (siStat1) to evaluate its protective effects.
  • FoxO1 was manipulated (silenced or overexpressed) in conjunction with Stat1 modulation.

Main Results:

  • High glucose reduced podocyte viability, increased apoptosis, and inhibited FoxO1 expression while upregulating Stat1.
  • Silencing Stat1 (siStat1) reversed high glucose-induced podocyte injury, decreasing apoptosis and ROS levels.
  • siStat1 upregulated antioxidant genes (Catalase, MnSOD, NQO1, HO1) and altered apoptosis-related proteins (Bax, Bcl-2).
  • Silencing FoxO1 counteracted the protective effects of siStat1.

Conclusions:

  • Stat1 silencing protects podocytes from high glucose-induced injury, including reduced viability, apoptosis, and ROS.
  • Stat1's function in high glucose injury may involve FoxO1-mediated nuclear oxidative stress.
  • Targeting Stat1 presents a potential therapeutic strategy for diabetic kidney disease.
Keywords:
FoxO1HGOxidative stressPodocyteStat1

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