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Estrogens inhibit TNF‐alpha induced apoptosis in an autoimmune disease: Sjogren's syndrome
Author(s) -
Chakraborty Rima,
Torres-Romero Luis Francisco,
Wang Yang,
McArthur Carole,
Molteni Agostino
Publication year - 2012
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.26.1_supplement.lb480
Subject(s) - tumor necrosis factor alpha , apoptosis , endocrinology , cytokine , cancer research , biology , gene expression , medicine , immunology , gene , biochemistry
Sjogrens Syndrome (SS) is a chronic autoimmune disease characterized by keratoconjunctivitis, salivary and lacrimal gland inflammation and rheumatoid arthritis. Tissue destruction in SS is related to cellular apoptosis and it may be clinically treated by glucocorticoids (dexamethasone). Tumor Necrosis Factor alpha (TNF‐α), a proapoptotic cytokine, is increased in SS. Reported here is the the effect of the estrogen E2 administration on TNF‐α induced apoptosis on cultures of human salivary gland (HSG) ductal cells. The cells were harvested after 4 hour culture in presence of a combination of TNF‐α and cycloheximide. Total RNA was extracted by RNA aqueous‐Midi total RNA isolation System (Ambion, Ca) and messenger RNA (MRNA) expression evaluated using selectively targeted gene microarrays on gene known to be involved on human apoptosis (GE arrays, S series) containing 67 genes. Results show a significant reduction of apoptotic activity of HSG cells treated with E2 when compared to controls. Using gene microarray analysis an up and down regulation of different apoptotic associated genes including RIPK2, TNFRF9, TNFRS6, TANK, BIl‐X, BCL2AI was observed. The data suggests that E2 plays a role on the apoptotic cell regulation, opening a potential therapy for this disease.