Sex, stroke, and inflammation: the potential for estrogen-mediated immunoprotection in stroke

Horm Behav. 2013 Feb;63(2):238-53. doi: 10.1016/j.yhbeh.2012.04.007. Epub 2012 Apr 24.

Abstract

Stroke is the third leading cause of death and the primary cause of disability in the developed world. Experimental and clinical data indicate that stroke is a sexually dimorphic disease, with males demonstrating an enhanced intrinsic sensitivity to ischemic damage throughout most of their lifespan. The neuroprotective role of estrogen in the female brain is well established, however, estrogen exposure can also be deleterious, especially in older women. The mechanisms for this remain unclear. Our current understanding is based on studies examining estrogen as it relates to neuronal injury, yet cerebral ischemia also induces a robust sterile inflammatory response involving local and systemic immune cells. Despite the potent anti-inflammatory effects of estrogen, few studies have investigated the contribution of estrogen to sex differences in the inflammatory response to stroke. This review examines the potential role for estrogen-mediated immunoprotection in ischemic injury.

Publication types

  • Review

MeSH terms

  • Brain Ischemia / genetics
  • Brain Ischemia / immunology
  • Brain Ischemia / therapy
  • Cytoprotection / drug effects*
  • Cytoprotection / genetics
  • Cytoprotection / physiology
  • Encephalitis* / etiology
  • Encephalitis* / genetics
  • Encephalitis* / immunology
  • Encephalitis* / prevention & control
  • Estrogens / pharmacology*
  • Estrogens / therapeutic use
  • Female
  • Humans
  • Immunity, Cellular / drug effects*
  • Immunity, Cellular / genetics
  • Immunity, Cellular / physiology
  • Male
  • MicroRNAs / genetics
  • MicroRNAs / physiology
  • Models, Biological
  • Sex Factors
  • Stroke* / etiology
  • Stroke* / genetics
  • Stroke* / immunology
  • Stroke* / physiopathology

Substances

  • Estrogens
  • MicroRNAs