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The MCP-1/CCR2 axis in podocytes is involved in apoptosis induced by diabetic conditions

Bo Young Nam1, Jisun Paeng, Seung Hye Kim

  • 1Department of Internal Medicine, College of Medicine, Severance Biomedical Science Institute, Yonsei University, Seodaemoon-Gu, Seoul, Korea.

Apoptosis : an International Journal on Programmed Cell Death
|October 19, 2011
PubMed

Insights

The MCP-1/CCR2 system and TGF-β1 contribute to podocyte apoptosis in diabetic nephropathy. Inhibiting CCR2 reduces high glucose-induced cell death and TGF-β1 levels, suggesting a therapeutic target.

Area of Science:

  • Nephrology
  • Molecular Biology
  • Immunology

Background:

  • Diabetic nephropathy involves inflammation, with monocyte chemoattractant protein-1 (MCP-1) playing a key role.
  • The direct impact of the MCP-1/CCR2 system on podocyte apoptosis in diabetes remains unclear.

Purpose of the Study:

  • To investigate the role of the MCP-1/CCR2 system in high glucose-induced podocyte apoptosis.
  • To explore the interplay between MCP-1/CCR2 and TGF-β1 in diabetic kidney disease.

Main Methods:

  • In vitro studies using mouse podocytes exposed to high glucose, MCP-1, or TGF-β1, with CCR2 inhibition (siRNA or RS102895).
  • In vivo studies using db/m and db/db mice treated with RS102895.
  • Western blot and TUNEL staining to assess apoptosis and cleaved caspase-3 expression.

Main Results:

  • CCR2 inhibition significantly reduced high glucose-induced podocyte apoptosis and TGF-β1 levels.
  • MCP-1 directly induced apoptosis via CCR2; TGF-β1-induced apoptosis was also ameliorated by CCR2 inhibition.
  • db/db mice showed increased glomerular apoptosis, which was attenuated by RS102895 treatment.

Conclusions:

  • The MCP-1/CCR2 system, in conjunction with TGF-β1, contributes to podocyte apoptosis in diabetic conditions.
  • Targeting the MCP-1/CCR2 pathway may offer a therapeutic strategy for diabetic nephropathy.

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