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[Effect of Par-4 on the apoptosis of islet β cell]

Xiaguang Gan1, Qi'nan Wu, Wuquan Deng

  • 1Department of Endocrinology, First Affi liated Hospital, Third Military Medical University, Chongqing 400038, China.

Zhong Nan Da Xue Xue Bao. Yi Xue Ban = Journal of Central South University. Medical Sciences
|February 6, 2015
PubMed
Abstract

Insights

High glucose and lipids increase islet cell apoptosis by upregulating prostate apoptosis response factor-4 (Par-4). Inhibiting Par-4 expression can improve this apoptosis, potentially by reducing endoplasmic reticulum stress.

Area of Science:

  • Endocrinology
  • Cell Biology
  • Molecular Medicine

Background:

  • High glucose and lipid levels are implicated in pancreatic islet cell dysfunction.
  • Prostate apoptosis response factor-4 (Par-4) plays a role in cellular apoptosis.
  • Endoplasmic reticulum stress is a known factor in beta-cell failure.

Purpose of the Study:

  • To investigate the impact of high glucose and lipid intervention on islet cell apoptosis.
  • To determine the role of prostate apoptosis response factor-4 (Par-4) in this process.
  • To elucidate the underlying mechanisms, including endoplasmic reticulum stress.

Main Methods:

  • Mouse islet beta cells (NIT-1) were treated with high glucose and fatty acids.
  • Par-4 expression was inhibited using specific interventions.
  • Cell apoptosis was assessed using TUNEL assay.
  • Protein levels of Par-4 and GRP78 were measured via Western blot.

Main Results:

  • High glucose and lipid intervention significantly increased islet beta cell apoptosis.
  • This increase was associated with elevated expression of Par-4 and GRP78.
  • Inhibiting Par-4 expression significantly reduced apoptosis and lowered Par-4 and GRP78 levels.

Conclusions:

  • Glucose and fatty acid-induced apoptosis of mouse islet beta cells can be ameliorated by inhibiting Par-4.
  • The protective effect may involve the reduction of endoplasmic reticulum stress.
  • Par-4 is a potential therapeutic target for managing islet cell apoptosis.

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