Myeloid-specific estrogen receptor {alpha} deficiency impairs metabolic homeostasis and accelerates atherosclerotic lesion development

  • Ribas V
  • Drew B
  • Le J
 et al. 
  • 1

    Readers

    Mendeley users who have this article in their library.
  • N/A

    Citations

    Citations of this article.

Abstract

ERalpha is expressed in macrophages and other immune cells known to exert dramatic effects on glucose homeostasis. We investigated the impact of ERalpha expression on macrophage function to determine whether hematopoietic or myeloid-specific ERalpha deletion manifests obesity-induced insulin resistance in mice. Indeed, altered plasma adipokine and cytokine levels, glucose intolerance, insulin resistance, and increased adipose tissue mass were observed in animals harboring a hematopoietic or myeloid-specific deletion of ERalpha. A similar obese phenotype and increased atherosclerotic lesion area was displayed in LDL receptor-KO mice transplanted with ERalpha(-/-) bone marrow. In isolated macrophages, ERalpha was necessary for repression of inflammation, maintenance of oxidative metabolism, IL-4-mediated induction of alternative activation, full phagocytic capacity in response to LPS, and oxidized LDL-induced expression of ApoE and Abca1. Furthermore, we identified ERalpha as a direct regulator of macrophage transglutaminase 2 expression, a multifunctional atheroprotective enzyme. Our findings suggest that diminished ERalpha expression in hematopoietic/myeloid cells promotes aspects of the metabolic syndrome and accelerates atherosclerosis in female mice

Author-supplied keywords

  • Animals
  • Atherosclerosis
  • Female
  • Hypertension
  • PM 2011 38
  • metabolism

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document

  • PMID: 21900603

Authors

  • V Ribas

  • B G Drew

  • J A Le

  • T Soleymani

  • P Daraei

  • D Sitz

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free