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Obligatory role for GPER in cardiovascular aging and disease

Matthias R Meyer1, Natalie C Fredette1, Christoph Daniel2

  • 1University of New Mexico Health Sciences Center, Department of Internal Medicine, Albuquerque, NM 87131, USA.

Science Signaling
|November 3, 2016
PubMed

Insights

Genetic deletion of G protein-coupled estrogen receptor (GPER) prevented aging-related cardiovascular disease by reducing NADPH oxidase (Nox1) and superoxide formation. Pharmacological GPER blockers (GRBs) also reduced hypertension by decreasing Nox1 activity.

Area of Science:

  • Cardiovascular Science
  • Endocrinology
  • Molecular Biology

Background:

  • G protein-coupled estrogen receptor (GPER) activation counteracts cardiovascular disease.
  • The role of GPER in aging-related cardiovascular pathologies was unexplored.
  • Genetic or pharmacological GPER inhibition was hypothesized to worsen cardiovascular disease.

Purpose of the Study:

  • To investigate the role of GPER in aging-related cardiovascular pathologies.
  • To determine the effect of GPER genetic ablation or pharmacological inhibition on cardiovascular disease.
  • To explore the underlying mechanisms involving NADPH oxidase (Nox) and superoxide (⋅O2-) formation.

Main Methods:

  • Genetic ablation of Gper in mice.
  • Pharmacological inhibition of GPER using G36 (GPER-selective blocker, GRB).
  • Assessment of Nox1 expression and ⋅O2- production in cells and mice exposed to angiotensin II.
  • Evaluation of arterial hypertension and cardiovascular pathologies.

Main Results:

  • Genetic ablation of Gper prevented aging-related cardiovascular pathologies in mice.
  • GPER deficiency reduced ⋅O2- formation by decreasing Nox1 expression.
  • Pharmacological GPER blockade with G36 decreased Nox1 abundance and ⋅O2- production, reducing angiotensin II-induced hypertension.

Conclusions:

  • GPER activity contributes to cardiovascular disease by regulating Nox1 expression and ⋅O2- production.
  • GPER blockers (GRBs) represent a potential therapeutic strategy for chronic diseases involving excessive ⋅O2- formation, such as hypertension and heart failure.

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