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C/EBP homologous protein induces mesangial cell apoptosis under hyperglycemia

Daqiang He1, Jianqiong Li, Jiayao Zhao

  • 1Department of Anatomy and Cell Biology, School of Medicine, Zhejiang University, Zhejiang 310058, P.R. China.

Molecular Medicine Reports
|December 18, 2012
PubMed

Insights

High glucose levels induce apoptosis in kidney mesangial cells via endoplasmic reticulum stress. C/EBP homologous protein (CHOP) activation plays a key role in this process, contributing to diabetic nephropathy development.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Endocrinology

Background:

  • Diabetes mellitus is a leading cause of kidney impairment.
  • The precise mechanisms underlying diabetic nephropathy remain incompletely understood.
  • Endoplasmic reticulum stress is implicated in cellular dysfunction during hyperglycemia.

Purpose of the Study:

  • To investigate the role of C/EBP homologous protein (CHOP) in hyperglycemia-induced mesangial cell apoptosis.
  • To elucidate the involvement of CHOP in endoplasmic reticulum stress-related kidney damage.

Main Methods:

  • Culturing human mesangial cells in normal and high glucose conditions.
  • Assessing apoptosis using TUNEL staining.
  • Quantifying CHOP and caspase-3 expression via immunohistochemistry and Western blot.

Main Results:

  • High glucose significantly increased TUNEL-positive mesangial cells.
  • CHOP and caspase-3 expression were significantly elevated in high glucose conditions.
  • These findings demonstrate CHOP's role in mediating apoptosis under hyperglycemia.

Conclusions:

  • CHOP mediates apoptosis in mesangial cells exposed to hyperglycemia.
  • CHOP activation is a significant factor in the pathogenesis of diabetic nephropathy.

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