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Tytuł pozycji:

Adiponectin Enhances B-Cell Proliferation and Differentiation via Activation of Akt1/STAT3 and Exacerbates Collagen-Induced Arthritis.

Tytuł:
Adiponectin Enhances B-Cell Proliferation and Differentiation via Activation of Akt1/STAT3 and Exacerbates Collagen-Induced Arthritis.
Autorzy:
Che N; Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Sun X; Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Gu L; Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wang X; Department of Pathology, Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.; Chongqing International Institute for Immunology, Hong Kong, China.
Shi J; Clinical Medical Science of the First Clinical Medical College, Nanjing Medical University, Nanjing, China.
Sun Y; Clinical Medical Science of the First Clinical Medical College, Nanjing Medical University, Nanjing, China.
Xu L; Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Liu R; Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Wang J; Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Zhu F; Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Peng N; Department of Rheumatology and Nephrology, The Second People's Hospital of China Three Gorges University, Yichang, China.
Xiao F; Department of Pathology, Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.; Chongqing International Institute for Immunology, Hong Kong, China.
Hu D; Department of Rheumatology and Nephrology, The Second People's Hospital of China Three Gorges University, Yichang, China.
Lu L; Department of Pathology, Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.; Chongqing International Institute for Immunology, Hong Kong, China.
Qiu W; Department of Immunology, Key Laboratory of Immunological Environment and Disease, Nanjing Medical University, Nanjing, China.
Zhang M; Department of Rheumatology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China.
Źródło:
Frontiers in immunology [Front Immunol] 2021 Mar 18; Vol. 12, pp. 626310. Date of Electronic Publication: 2021 Mar 18 (Print Publication: 2021).
Typ publikacji:
Journal Article; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: [Lausanne : Frontiers Research Foundation]
MeSH Terms:
Adiponectin/*toxicity
Arthritis, Experimental/*enzymology
B-Lymphocytes/*drug effects
Cell Differentiation/*drug effects
Cell Proliferation/*drug effects
Lymphocyte Activation/*drug effects
Proto-Oncogene Proteins c-akt/*metabolism
STAT3 Transcription Factor/*metabolism
Animals ; Arthritis, Experimental/chemically induced ; Arthritis, Experimental/immunology ; Arthritis, Experimental/pathology ; B-Lymphocytes/enzymology ; B-Lymphocytes/immunology ; Collagen Type II ; Enzyme Activation ; Male ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Phosphatidylinositol 3-Kinase/metabolism ; Positive Regulatory Domain I-Binding Factor 1/genetics ; Positive Regulatory Domain I-Binding Factor 1/metabolism ; Proto-Oncogene Proteins c-akt/genetics ; Receptors, Adiponectin/agonists ; Receptors, Adiponectin/genetics ; Receptors, Adiponectin/metabolism ; STAT3 Transcription Factor/genetics ; Signal Transduction ; Mice
References:
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Contributed Indexing:
Keywords: B cells; adiponectin; collagen-induced arthritis; differentiation; proliferation
Substance Nomenclature:
0 (Adiponectin)
0 (Adipoq protein, mouse)
0 (Collagen Type II)
0 (Prdm1 protein, mouse)
0 (Receptors, Adiponectin)
0 (STAT3 Transcription Factor)
0 (Stat3 protein, mouse)
0 (adiponectin receptor 1, mouse)
EC 2.1.1.- (Positive Regulatory Domain I-Binding Factor 1)
EC 2.7.1.137 (Phosphatidylinositol 3-Kinase)
EC 2.7.11.1 (Akt1 protein, mouse)
EC 2.7.11.1 (Proto-Oncogene Proteins c-akt)
Entry Date(s):
Date Created: 20210405 Date Completed: 20210915 Latest Revision: 20240226
Update Code:
20240226
PubMed Central ID:
PMC8012765
DOI:
10.3389/fimmu.2021.626310
PMID:
33815378
Czasopismo naukowe
Although B cells have been shown to contribute to the pathogenesis of rheumatoid arthritis (RA), the precise role of B cells in RA needs to be explored further. Our previous studies have revealed that adiponectin (AD) is expressed at high levels in inflamed synovial joint tissues, and its expression is closely correlated with progressive bone erosion in patients with RA. In this study, we investigated the possible role of AD in B cell proliferation and differentiation. We found that AD stimulation could induce B cell proliferation and differentiation in cell culture. Notably, local intraarticular injection of AD promoted B cell expansion in joint tissues and exacerbated arthritis in mice with collagen-induced arthritis (CIA). Mechanistically, AD induced the activation of PI3K/Akt1 and STAT3 and promoted the proliferation and differentiation of B cells. Moreover, STAT3 bound to the promoter of the Blimp-1 gene, upregulated Blimp-1 expression at the transcriptional level, and promoted B cell differentiation. Collectively, we observed that AD exacerbated CIA by enhancing B cell proliferation and differentiation mediated by the PI3K/Akt1/STAT3 axis.
Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
(Copyright © 2021 Che, Sun, Gu, Wang, Shi, Sun, Xu, Liu, Wang, Zhu, Peng, Xiao, Hu, Lu, Qiu and Zhang.)

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