Paper Information

Title: 

ESTROGEN INDUCED APOPTOTIC PATHWAY IN PATIENTS WITH SYSTEMIC LUPUS ERYTHEMATOSUS

Type: POSTER
Author(s): RASTIN M.,HATEF M.,TABASI N.A.,SHEYKH A.,MORAD ABBASI J.,MAHMOUDI M.
 
 
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2007Volume 18
 
 
Abstract: 

Introduction: Systemic lupus erythematosus is an autoimmune disease which mostly occurs in women during their childbearing years. The strongest risk factor for development of SLE is female gender and hormones. Estrogen enhances immune responses and in SLE pathogenesis it is important to understand how nuclear antigens become immunogenic because for development of the disease nuclear antigens have to be accessible to immune system. Apoptotic cells are potential reservoirs of altered auto antigens. In promoter region of some genes such as FasL there is an estrogen responsive element, which binds estrogen and induces apoptosis and of apoptosis molecules gene expression via activation of death receptor. In this study we investigated the molecular mechanisms of the effects of estrogen apoptotic related molecules on T lymphocytes in SLE patients in gene expression levels.
Methods: Study group comprised of 35 SLE patients, and 20 age and sex matched controls. T lymphocytes cultured with estrogen. For detecting gene expression, RNA was isolated from cells, cDNA synthesized and using specific primers the expression levels of Fas, FasL, Bcl-2, Caspase 8 and Caspase 9 were determined.
Results
and Conclusion: Estrogen induced Fas/FasL pathway apoptosis in lupus patients, which is accompanied by significant enhancement of FasL and Caspase 8 genes expression levels and significant increased percent of apoptotic cells (p<0.05), which implies more susceptibility of patients to estrogen. There were no significant changes in expression levels of Fas, Bcl-2 and Caspase 9 genes.

 
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