Gαq Regulates the Development of Rheumatoid Arthritis by Modulating Th1 Differentiation
The Gαq-containing G protein, an important member of Gq/11 class, is ubiquitously expressed in mammalian cells. Gαq has been found to play an important role in immune regulation and development of autoimmune disease such as rheumatoid arthritis (RA). However, how Gαq participates in the pathogenesis...
Saved in:
| Main Authors: | , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2017-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2017/4639081 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832560386637824000 |
|---|---|
| author | Dashan Wang Yuan Liu Yan Li Yan He Jiyun Zhang Guixiu Shi |
| author_facet | Dashan Wang Yuan Liu Yan Li Yan He Jiyun Zhang Guixiu Shi |
| author_sort | Dashan Wang |
| collection | DOAJ |
| description | The Gαq-containing G protein, an important member of Gq/11 class, is ubiquitously expressed in mammalian cells. Gαq has been found to play an important role in immune regulation and development of autoimmune disease such as rheumatoid arthritis (RA). However, how Gαq participates in the pathogenesis of RA is still not fully understood. In the present study, we aimed to find out whether Gαq controls RA via regulation of Th1 differentiation. We observed that the expression of Gαq was negatively correlated with the expression of signature Th1 cytokine (IFN-γ) in RA patients, which suggests a negative role of Gαq in differentiation of Th1 cells. By using Gαq knockout (Gnaq−/−) mice, we demonstrated that loss of Gαq led to enhanced Th1 cell differentiation. Gαq negative regulated the differentiation of Th1 cell by modulating the expression of T-bet and the activity of STAT4. Furthermore, we detected the increased ratio of Th1 cells in Gnaq−/− bone marrow (BM) chimeras spontaneously developing inflammatory arthritis. In conclusion, results presented in the study demonstrate that loss of Gαq promotes the differentiation of Th1 cells and contributes to the pathogenesis of RA. |
| format | Article |
| id | doaj-art-647c763301554358be257be771681550 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2017-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-647c763301554358be257be7716815502025-02-03T01:27:45ZengWileyMediators of Inflammation0962-93511466-18612017-01-01201710.1155/2017/46390814639081Gαq Regulates the Development of Rheumatoid Arthritis by Modulating Th1 DifferentiationDashan Wang0Yuan Liu1Yan Li2Yan He3Jiyun Zhang4Guixiu Shi5Molecular Biology Research Center, Key Medical Health Laboratory for Laboratory Medicine of Shandong Province, Department of Laboratory Medicine, Shandong Medical College, Linyi, Shandong 276000, ChinaDepartment of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003, ChinaDepartment of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003, ChinaDepartment of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003, ChinaKey Medical Health Laboratory for Laboratory Medicine of Shandong Province, Department of Laboratory Medicine, Shandong Medical College, Linyi, Shandong 276000, ChinaDepartment of Rheumatology and Clinical Immunology, The First Affiliated Hospital of Xiamen University, Xiamen, Fujian 361003, ChinaThe Gαq-containing G protein, an important member of Gq/11 class, is ubiquitously expressed in mammalian cells. Gαq has been found to play an important role in immune regulation and development of autoimmune disease such as rheumatoid arthritis (RA). However, how Gαq participates in the pathogenesis of RA is still not fully understood. In the present study, we aimed to find out whether Gαq controls RA via regulation of Th1 differentiation. We observed that the expression of Gαq was negatively correlated with the expression of signature Th1 cytokine (IFN-γ) in RA patients, which suggests a negative role of Gαq in differentiation of Th1 cells. By using Gαq knockout (Gnaq−/−) mice, we demonstrated that loss of Gαq led to enhanced Th1 cell differentiation. Gαq negative regulated the differentiation of Th1 cell by modulating the expression of T-bet and the activity of STAT4. Furthermore, we detected the increased ratio of Th1 cells in Gnaq−/− bone marrow (BM) chimeras spontaneously developing inflammatory arthritis. In conclusion, results presented in the study demonstrate that loss of Gαq promotes the differentiation of Th1 cells and contributes to the pathogenesis of RA.http://dx.doi.org/10.1155/2017/4639081 |
| spellingShingle | Dashan Wang Yuan Liu Yan Li Yan He Jiyun Zhang Guixiu Shi Gαq Regulates the Development of Rheumatoid Arthritis by Modulating Th1 Differentiation Mediators of Inflammation |
| title | Gαq Regulates the Development of Rheumatoid Arthritis by Modulating Th1 Differentiation |
| title_full | Gαq Regulates the Development of Rheumatoid Arthritis by Modulating Th1 Differentiation |
| title_fullStr | Gαq Regulates the Development of Rheumatoid Arthritis by Modulating Th1 Differentiation |
| title_full_unstemmed | Gαq Regulates the Development of Rheumatoid Arthritis by Modulating Th1 Differentiation |
| title_short | Gαq Regulates the Development of Rheumatoid Arthritis by Modulating Th1 Differentiation |
| title_sort | gαq regulates the development of rheumatoid arthritis by modulating th1 differentiation |
| url | http://dx.doi.org/10.1155/2017/4639081 |
| work_keys_str_mv | AT dashanwang gaqregulatesthedevelopmentofrheumatoidarthritisbymodulatingth1differentiation AT yuanliu gaqregulatesthedevelopmentofrheumatoidarthritisbymodulatingth1differentiation AT yanli gaqregulatesthedevelopmentofrheumatoidarthritisbymodulatingth1differentiation AT yanhe gaqregulatesthedevelopmentofrheumatoidarthritisbymodulatingth1differentiation AT jiyunzhang gaqregulatesthedevelopmentofrheumatoidarthritisbymodulatingth1differentiation AT guixiushi gaqregulatesthedevelopmentofrheumatoidarthritisbymodulatingth1differentiation |