Open Access全身性紅斑狼瘡之二羥雌激素調升蛋白質磷酸酶 3 CA之表現是經由雌激素受體α基因之過度表現
Author(s) -
Lin HuiLi,
Yen JengHsien,
Chiou ShiShin,
Tsai WenChan,
Ou TsanTeng,
Wu ChengChin,
Liu HongWen
Publication year - 2011
Publication title -
the kaohsiung journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.439
H-Index - 36
eISSN - 2410-8650
pISSN - 1607-551X
DOI - 10.1016/j.kjms.2010.12.005
Subject(s) - calcineurin , endocrinology , medicine , estrogen , estrogen receptor alpha , estrogen receptor , gene expression , messenger rna , immunology , gene , biology , transplantation , biochemistry , cancer , breast cancer
Systemic lupus erythematosus (SLE) is an autoimmune disease primarily affecting women (9:1 compared with men). To investigate the influence of female sex hormone estrogen on the development of female‐biased lupus, we compared the expression of estrogen receptor alpha (ERα) gene and protein levels as well as expression of T‐cell activation gene calcineurin in response to estrogen in peripheral blood lymphocytes (PBLs) from SLE patients and normal controls. PBLs were isolated from 20 female SLE patients and 6 normal female controls. The amount of ERα protein in PBL was measured by flow cytometry. The expression of ERα and calcineurin messenger RNA was measured by semi‐quantitative reverse transcription‐polymerase chain reaction. Calcineurin phosphatase activity was measured by calcineurin assay kit. The expression of ERα messenger RNA and ERα protein was significantly increased ( p = 0.001 and p = 0.023, respectively) in PBL from SLE patients compared with that from normal controls. In addition, the basal calcineurin in PBL from SLE patients was significantly higher ( p = 0.000) than that from normal controls, and estrogen‐induced expression of calcineurin was increased ( p = 0.007) in PBL from SLE patients compared with that from normal controls, a 3.15‐fold increase. This increase was inhibited by the ERα antagonism ICI 182,780. The effects of ER antagonism were also found in calcineurin activity. These data suggest that overexpression of ERα gene and enhanced activation of calcineurin in response to estrogen in PBL may contribute to the pathogenesis of female dominant in SLE.