title: Expression of G protein αq Subunit is Decreased in Lymphocytes from Patients with Rheumatoid Arthritis and is Correlated with Disease Activity.
abstract: Gαq, 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 Gαq in their immune system could spontaneously develop inflammatory arthritis. In this study, we showed that the Gαq 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 Gαq 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 Gαq controlled the apoptosis of RA PBLs through regulating the activity of Mcl-1 and caspase-3. These data suggested that Gαq might be involved in the pathogenesis of RA by regulating PBLs apoptosis.
authors.affiliation: Division of Rheumatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaGLP Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.affiliation: Division of Rheumatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaGLP Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.affiliation: Division of Rheumatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaGLP Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
authors.forename: Y
authors.initials: Y
authors.lastname: He
authors.affiliation: Division of Rheumatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaGLP Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Sun
authors.affiliation: Division of Rheumatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaGLP Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
authors.forename: W
authors.initials: W
authors.lastname: Sun
authors.affiliation: Division of Rheumatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaGLP Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
authors.forename: Q
authors.initials: Q
authors.lastname: Xie
authors.affiliation: Division of Rheumatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaGLP Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
authors.forename: G
authors.initials: G
authors.lastname: Yin
authors.affiliation: Division of Rheumatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaGLP Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
authors.forename: Y
authors.initials: Y
authors.lastname: Du
authors.affiliation: Division of Rheumatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaGLP Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
authors.forename: L
authors.initials: L
authors.lastname: Wang
authors.affiliation: Division of Rheumatology, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, ChinaGLP Center, State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
authors.forename: G
authors.initials: G
authors.lastname: Shi
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000235:genetics / Q000276:immunology; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D001323:Autoantibodies / Q000097:blood / Q000276:immunology; D002097:C-Reactive Protein / Q000276:immunology / Q000378:metabolism; D016022:Case-Control Studies; D053148:Caspase 3 / Q000235:genetics / Q000276:immunology; D005260:Female; D043802:GTP-Binding Protein alpha Subunits, Gq-G11 / Q000235:genetics* / Q000276:immunology; D005786:Gene Expression Regulation; D006801:Humans; D007963:Leukocytes, Mononuclear / Q000276:immunology* / Q000473:pathology; D008297:Male; D008875:Middle Aged; D064549:Myeloid Cell Leukemia Sequence 1 Protein / Q000235:genetics / Q000276:immunology; D010456:Peptides, Cyclic / Q000235:genetics / Q000276:immunology; D019869:Phosphatidylinositol 3-Kinases / Q000235:genetics / Q000276:immunology; D061251:Primary Cell Culture; D012333:RNA, Messenger / Q000235:genetics* / Q000276:immunology; D012217:Rheumatoid Factor / Q000235:genetics / Q000276:immunology; D012720:Severity of Illness Index; D015398:Signal Transduction
chemical_list: D001323:Autoantibodies; C579095:MCL1 protein, human; D064549:Myeloid Cell Leukemia Sequence 1 Protein; D010456:Peptides, Cyclic; D012333:RNA, Messenger; C487763:cyclic citrullinated peptide; D002097:C-Reactive Protein; D012217:Rheumatoid Factor; D019869:Phosphatidylinositol 3-Kinases; D053148:Caspase 3; D043802:GTP-Binding Protein alpha Subunits, Gq-G11