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(Pro)renin receptor: another member of the system controlled by angiotensin II?

Luciana G Pereira1, Carine P Arnoni, Edgar Maquigussa

  • 1Department of Medicine, Renal Division, Federal University of São Paulo, São Paulo, Brazil.

Journal of the Renin-Angiotensin-Aldosterone System : JRAAS
|October 15, 2011
PubMed

Insights

High glucose increases prorenin receptor [(P)RR] in diabetic kidneys, driving fibrosis. Intracellular angiotensin II (AngII) and (P)RR activation mediate this process, offering new therapeutic targets.

Area of Science:

  • Nephrology
  • Diabetology
  • Molecular Biology

Background:

  • The prorenin receptor [(P)RR] is upregulated in diabetic kidneys.
  • High glucose (HG) induces profibrotic molecule overproduction in mesangial cells (MCs), mediated by ERK1/2 phosphorylation.
  • Mechanisms of HG-induced (P)RR gene expression are unclear.

Purpose of the Study:

  • Evaluate the role of intracellular angiotensin II (AngII) in (P)RR gene expression and function.
  • Investigate HG-induced (P)RR regulation in human MCs (HMCs).

Main Methods:

  • Used an in vitro system with HMCs stimulated by HG.
  • Compared effects of AT1 receptor blockers (losartan, candesartan) and (P)RR mRNA silencing (siRNA).

Main Results:

  • HG increased (P)RR, fibronectin expression, and ERK1/2 phosphorylation.
  • These effects were reversed by (P)RR siRNA and losartan.
  • Candesartan did not reverse the effects, suggesting a role for AT1 receptor internalization.

Conclusions:

  • Intracellular AngII may control (P)RR gene activity.
  • (P)RR activation is a primary driver of HG-induced ERK1/2 phosphorylation and fibronectin overproduction.
  • The AngII-(P)RR relationship presents a novel pathway for MC dysfunction in diabetic kidneys.

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