The pathway of estradiol-induced apoptosis in patients with systemic lupus erythematosus

Clin Rheumatol. 2012 Mar;31(3):417-24. doi: 10.1007/s10067-011-1821-3. Epub 2011 Aug 12.

Abstract

Systemic lupus erythematosus (SLE) is a disease with unknown etiology. The pathologic role of sex hormones and apoptosis in SLE has often been discussed. We studied the effects of estradiol in the pathway of induced apoptosis in Iranian SLE patients. T lymphocytes from 35 SLE patients and 20 age-matched controls were isolated and cultured in the presence of 10(-8) M 17-β estradiol. The expression levels of Fas, Fas ligand (FasL), Bcl-2, caspase-8, and caspase-9 mRNAs were determined semiquantitatively in comparison to the expression level of beta actin RNA. Estradiol exposure did not have any significant effects on the expression levels of Fas, Bcl-2, and caspase-9 in SLE patients and controls. However, the expression levels of FasL and caspase-8 were significantly increased in SLE patients, but not in controls. This suggests the probable involvement of extrinsic apoptosis pathway in estradiol-induced apoptosis in SLE.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Adult
  • Apoptosis / drug effects*
  • Apoptosis / physiology
  • Caspase 8 / metabolism
  • Caspase 9 / metabolism
  • Cells, Cultured
  • Estradiol / pharmacology*
  • Fas Ligand Protein / metabolism
  • Female
  • Humans
  • Lupus Erythematosus, Systemic / metabolism*
  • Male
  • Middle Aged
  • T-Lymphocytes / drug effects*
  • T-Lymphocytes / metabolism
  • fas Receptor / metabolism

Substances

  • Fas Ligand Protein
  • fas Receptor
  • Estradiol
  • Caspase 8
  • Caspase 9