中国科学院机构知识库网格
Chinese Academy of Sciences Institutional Repositories Grid
SGK1-FoxO1 Signaling Pathway Mediates Th17/Treg Imbalance and Target Organ Inflammation in Angiotensin II-Induced Hypertension

文献类型:期刊论文

作者Du, Ya-Nan1,3; Tang, Xiao-Feng1,3; Xu, Lian3; Chen, Wen-Dong1,3; Gao, Ping-Jin1,2,3; Han, Wei-Qing1,2,3; Xu, Lian2; ,
刊名FRONTIERS IN PHYSIOLOGY
出版日期2018
卷号9期号:-页码:1581
关键词serum/glucocorticoid regulated kinase 1 Th17 cells Treg cells target organ damage angiotensin II
ISSN号1664-042X
DOI10.3389/fphys.2018.01581
文献子类Article
英文摘要It has been demonstrated that serum/glucocorticoid regulated kinase 1 (SGK1) and the downstream transcription factor forkhead box O1 (FoxO1) plays a critical role in the differentiation of T helper 17 cells/regulatory T cells (Th17/Treg). In the present study, we hypothesized that this SGK1-FoxO1 signaling pathway is involved in Th17/Treg imbalance and target organ damage in angiotensin II (AngII)-induced hypertensive mice. Results show that SGK1 inhibitor EMD638683 significantly reversed renal dysfunction and cardiac dysfunction in echocardiography as indicated by decreased blood urine nitrogen and serum creatinine in AngII-infused mice. Flow cytometric assay shows that there was significant Th17/Treg imbalance in spleen and in renal/cardiac infiltrating lymphocytes as indicated by the increased Th17 cells (CD4(+)-IL17A(+) cells) and decreased Treg cells (CD4(+)-Foxp3(+)). Consistently, real-time PCR shows that Th17-related cytokines including IL-17A, IL-23, and tumor necrosis factor alpha (TNF-alpha) was increased and Treg-related cytokine IL-10 was decreased in renal and cardiac infiltrating lymphocytes in AngII-infused mice. Meanwhile, SGK1 protein level, as well as its phosphorylation and activity, was significantly increased in spleen in AngII-infused rats. Furthermore, it was found that splenic phosphorylated FoxO1 was significantly increased, whereas total FoxO1 in nuclear preparation was significantly decreased in AngII-infused mice, suggesting that increased FoxO1 phosphorylation initiate its translocation from cytoplasm to nucleus. Notably, all changes were significantly inhibited by the treatment of EMD638683. These results suggest that SGK1 was involved in Th17/Treg imbalance and target organ damage in AngII-induced hypertension.
学科主题Physiology
WOS关键词REGULATORY T-CELLS ; KINASE 1 ; AORTIC-ANEURYSM ; TUBULAR CELLS ; KNOCKOUT MICE ; GROWTH-FACTOR ; ACTIVATION ; SERUM ; SGK1 ; EXPRESSION
语种英语
WOS记录号WOS:000450193300001
出版者FRONTIERS MEDIA SA
版本出版稿
源URL[http://202.127.25.144/handle/331004/854]  
专题中国科学院上海生命科学研究院营养科学研究所
作者单位1.Shanghai Res Inst Hypertens, Shanghai, Peoples R China;
2.Chinese Acad Sci, Lab Vasc Biol, Shanghai Inst Biol Sci, Inst Hlth Sci, Shanghai, Peoples R China,
3.Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Key Lab Hypertens, Sch Med, Shanghai, Peoples R China;
推荐引用方式
GB/T 7714
Du, Ya-Nan,Tang, Xiao-Feng,Xu, Lian,et al. SGK1-FoxO1 Signaling Pathway Mediates Th17/Treg Imbalance and Target Organ Inflammation in Angiotensin II-Induced Hypertension[J]. FRONTIERS IN PHYSIOLOGY,2018,9(-):1581.
APA Du, Ya-Nan.,Tang, Xiao-Feng.,Xu, Lian.,Chen, Wen-Dong.,Gao, Ping-Jin.,...&,.(2018).SGK1-FoxO1 Signaling Pathway Mediates Th17/Treg Imbalance and Target Organ Inflammation in Angiotensin II-Induced Hypertension.FRONTIERS IN PHYSIOLOGY,9(-),1581.
MLA Du, Ya-Nan,et al."SGK1-FoxO1 Signaling Pathway Mediates Th17/Treg Imbalance and Target Organ Inflammation in Angiotensin II-Induced Hypertension".FRONTIERS IN PHYSIOLOGY 9.-(2018):1581.

入库方式: OAI收割

来源:上海营养与健康研究所

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