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Advanced glycation end-products reduce podocyte adhesion by activating the renin-angiotensin system and increasing

Cailian Cheng1, Zhenda Zheng, Chenggang Shi

  • 1Department of Nephrology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong 510630, P.R. China.

Experimental and Therapeutic Medicine
|November 21, 2013
PubMed

Insights

Advanced glycation end-products (AGEs) reduce kidney podocyte adhesion by increasing integrin-linked kinase (ILK) expression. Losartan partially reversed this effect, suggesting the renin-angiotensin system

Area of Science:

  • Nephrology
  • Molecular Biology
  • Biochemistry

Background:

  • Podocyte injury is a key factor in diabetic nephropathy.
  • Advanced glycation end-products (AGEs) are implicated in diabetic kidney disease pathogenesis.
  • The precise mechanisms by which AGEs affect podocyte function remain incompletely understood.

Purpose of the Study:

  • To investigate the impact of AGEs on podocyte adhesion.
  • To elucidate the role of integrin-linked kinase (ILK) in AGE-induced podocyte dysfunction.
  • To explore the involvement of the renin-angiotensin system (RAS) in these processes.

Main Methods:

  • Primary mouse podocytes were treated with AGEs or control (bovine serum albumin).
  • Podocyte adhesion was quantified using a hexosaminidase assay.
  • Integrin-linked kinase (ILK) expression was assessed via qPCR and Western blotting.
  • The effect of losartan, an angiotensin II receptor blocker, was evaluated.

Main Results:

  • AGEs significantly reduced podocyte adhesion in a dose-dependent manner.
  • AGE exposure led to a concentration-dependent increase in ILK expression.
  • Losartan pretreatment mitigated ILK upregulation and partially restored podocyte adhesion.
  • However, losartan-treated podocytes still exhibited reduced adhesion compared to controls.

Conclusions:

  • AGEs impair podocyte adhesion through the upregulation of ILK.
  • This effect is partly mediated by the activation of the renin-angiotensin system within podocytes.
  • Targeting the RAS may offer a therapeutic strategy for AGE-induced podocyte injury.
Keywords:
adhesionadvanced glycation end-productsintegrin-linked kinasepodocyte

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