Expression of G protein aq Subunit is Decreased in Lymphocytes from Patients with Rheumatoid Arthritis and is Correlated with Disease Activity

被引:15
作者
Wang, Y. [1 ,2 ]
Li, Y. [1 ]
He, Y. [1 ]
Sun, Y. [1 ]
Sun, W. [1 ]
Xie, Q. [1 ]
Yin, G. [1 ]
Du, Y. [2 ]
Wang, L. [2 ]
Shi, G. [1 ]
机构
[1] Sichuan Univ, W China Hosp, State Key Lab Biotherapy, Div Rheumatol, Chengdu 610041, Peoples R China
[2] Sichuan Univ, W China Hosp, State Key Lab Biotherapy, GLP Ctr, Chengdu 610041, Peoples R China
基金
中国国家自然科学基金;
关键词
G-ALPHA-Q; HEART-FAILURE; CARDIAC-HYPERTROPHY; SIGNALING PATHWAYS; PHOSPHOLIPASE-C; APOPTOSIS; CRITERIA; THERAPY; CELLS; GENE;
D O I
10.1111/j.1365-3083.2011.02635.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Gaq, the alpha subunit of Gq, a member of the Gq/11 sub-family, was reported to inhibit phosphatidylinositol-3-Kinase (PI3K) activation and prevent the activation of Akt. Previous studies demonstrated that mice losing Gaq in their immune system could spontaneously develop inflammatory arthritis. In this study, we showed that the Gaq expressions at mRNA and protein levels in the peripheral blood lymphocytes (PBLs) from patients with rheumatoid arthritis (RA) were significantly decreased in comparison of which in healthy individuals. The expression levels of Gaq mRNA in PBLs from patients with RA were correlated with RA disease activity (DAS28), anti-cyclic citrullinated protein antibodies, C-reactive protein and rheumatoid factor. We also demonstrated that Gaq controlled the apoptosis of RA PBLs through regulating the activity of Mcl-1 and caspase-3. These data suggested that Gaq might be involved in the pathogenesis of RA by regulating PBLs apoptosis.
引用
收藏
页码:203 / 209
页数:7
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