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Podocytes of AT2 receptor knockout mice are protected from angiotensin II-mediated RAGE induction

Christiane Rüster1, Sybille Franke, Ulrich Wenzel

  • 1Klinik für Innere Medizin III, Friedrich Schiller University, Erlanger-Allee 101, Jena, Germany. Gunter.Wolf@med.uni-jena.de

American Journal of Nephrology
|August 18, 2011
PubMed
Abstract

Insights

Angiotensin II (ANG II) induces receptor for advanced glycation end products (RAGE) in kidney podocytes through AT2 receptors. This pathway is crucial in diabetic nephropathy and may not be targeted by AT1 receptor blockers.

Area of Science:

  • Nephrology
  • Endocrinology
  • Molecular Biology

Background:

  • Advanced glycation end products (AGEs) and their receptor (RAGE) are implicated in diabetic nephropathy.
  • Previous in vitro studies indicated angiotensin II (ANG II) induces RAGE via AT2 receptors in podocytes.

Purpose of the Study:

  • To validate the in vivo role of AT2 receptors in ANG II-induced RAGE expression in diabetic nephropathy.

Main Methods:

  • Utilized AT2 receptor knockout (AT2(-/-)) and wild-type mice infused with ANG II for 14 days.
  • Assessed RAGE and Nε-carboxymethyllysine expression in renal podocytes via immunohistochemistry.
  • Analyzed glomerular AT1a receptor expression and RAGE mRNA levels using real-time PCR.

Main Results:

  • ANG II significantly increased podocyte RAGE expression in wild-type mice, but only moderately in AT2(-/-) mice.
  • Similar patterns were observed for the AGE Nε-carboxymethyllysine.
  • No significant changes in AT1a receptor expression or glomerular apoptosis were noted; RAGE mRNA levels in whole kidney were comparable between groups.

Conclusions:

  • Podocyte RAGE induction by ANG II is mediated through AT2 receptors in vivo.
  • These findings suggest AT1 receptor blockers may not fully address all ANG II-driven changes in diabetic nephropathy.

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