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Angiotensin II upregulates RAGE expression on podocytes: role of AT2 receptors

Christiane Rüster1, Tzvetanka Bondeva, Sybille Franke

  • 1Klinik für Innere Medizin III, Friedrich Schiller University, Jena, Germany.

American Journal of Nephrology
|January 9, 2009
PubMed
Abstract

Insights

Angiotensin II (ANG II) upregulates advanced glycation end product (AGE) receptor (RAGE) in podocytes via AT2 receptors. This interaction may worsen diabetic nephropathy by increasing inflammation and podocyte injury.

Area of Science:

  • Nephrology
  • Endocrinology
  • Molecular Biology

Background:

  • Advanced glycation end products (AGEs) are implicated in diabetic nephropathy.
  • The receptor for AGEs (RAGE) is expressed on podocytes.
  • The role of angiotensin II (ANG II) in modulating RAGE expression in podocytes is unclear.

Purpose of the Study:

  • To investigate whether ANG II modulates RAGE expression in cultured differentiated podocytes.
  • To elucidate the receptor subtype and signaling pathways involved in ANG II-mediated RAGE modulation.
  • To determine the functional consequences of altered RAGE expression.

Main Methods:

  • Cultured differentiated podocytes were treated with ANG II.
  • RAGE mRNA and protein expression were assessed.
  • Reporter constructs were used to analyze RAGE promoter activity.
  • Tumor necrosis factor-alpha expression and AGE-BSA uptake were measured.

Main Results:

  • ANG II induced RAGE mRNA and protein expression via AT2 receptors, independent of proliferation or protein content.
  • Transcriptional activity, specifically involving an NF-kappaB binding site, was essential for ANG II-induced RAGE upregulation.
  • ANG II preincubation enhanced AGE-induced tumor necrosis factor-alpha expression, indicating functional consequences.
  • ANG II did not affect AGE-BSA uptake or induce apoptosis.

Conclusions:

  • A significant interaction exists between the renin-angiotensin system and the AGE/RAGE axis in podocytes.
  • Increased intraglomerular ANG II in diabetic nephropathy may exacerbate podocyte injury and inflammation via RAGE.
  • This interaction highlights a potential therapeutic target for diabetic nephropathy.

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