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Tytuł:
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Upregulated TSG-6 Expression in ADSCs Inhibits the BV2 Microglia-Mediated Inflammatory Response.
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Autorzy:
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Hu Y; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan Hubei 430030, China.
Li G; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan Hubei 430030, China.
Zhang Y; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan Hubei 430030, China.
Liu N; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan Hubei 430030, China.
Zhang P; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan Hubei 430030, China.
Pan C; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan Hubei 430030, China.
Nie H; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan Hubei 430030, China.
Li Q; Department of Neurology, The First Affiliated Hospital of Chongqing Medical University, Chongqing 400016, China.
Tang Z; Department of Neurology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan Hubei 430030, China.
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Źródło:
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BioMed research international [Biomed Res Int] 2018 Nov 21; Vol. 2018, pp. 7239181. Date of Electronic Publication: 2018 Nov 21 (Print Publication: 2018).
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Typ publikacji:
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Journal Article
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Język:
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English
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Imprint Name(s):
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Original Publication: New York, NY : Hindawi Pub. Co.
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MeSH Terms:
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Adipocytes/*metabolism
Cell Adhesion Molecules/*metabolism
Inflammation/*metabolism
Microglia/*metabolism
Stem Cells/*metabolism
Adipocytes/drug effects ; Animals ; Cell Line ; Cytokines/metabolism ; Female ; Inflammation/chemically induced ; Interleukin-1beta/metabolism ; Interleukin-6/metabolism ; Lipopolysaccharides/pharmacology ; MicroRNAs/metabolism ; Microglia/drug effects ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Stem Cells/drug effects ; Tumor Necrosis Factor-alpha/metabolism ; Up-Regulation/drug effects
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References:
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Substance Nomenclature:
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0 (Cell Adhesion Molecules)
0 (Cytokines)
0 (Interleukin-1beta)
0 (Interleukin-6)
0 (Lipopolysaccharides)
0 (MicroRNAs)
0 (RNA, Messenger)
0 (Tnfaip6 protein, rat)
0 (Tumor Necrosis Factor-alpha)
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Entry Date(s):
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Date Created: 20181226 Date Completed: 20190408 Latest Revision: 20220330
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Update Code:
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20240105
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PubMed Central ID:
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PMC6280241
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DOI:
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10.1155/2018/7239181
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PMID:
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30584538
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Objectives: The microglial cells are immune surveillance cells in the central nervous system and can be activated during neurological disorders. Adipose-derived stem cells (ADSCs) were reported to inhibit the inflammatory response in microglia by secreting proteins like tumor necrosis factor-inducible gene 6 protein (TSG-6). We aim to explore the mechanisms and the associated microRNAs.
Methods: ADSCs were cultured and TSG-6 expression was evaluated. ADSCs were cocultured with lipopolysaccharide- (LPS-) induced BV2 microglia and the supernatant was harvested for detecting cytokines. The total RNA was extracted and sequenced by high-throughput sequencing. MicroRNA profiles were compared between two treatment groups of ADSCs. A comprehensive bioinformatics analysis and confirmation experiments were performed to identify the microRNAs targeting at TSG-6.
Results: We found that ADSCs could secrete TSG-6 to inhibit the proinflammatory cytokines, including interleukin-1 beta and interleukin-6, and tumor necrosis factor alpha (TNF α ), produced by LPS-induced microglia-mediated inflammatory response. Bioinformatics analysis showed a total of 35 microRNAs differentially expressed between the two groups of ADSCs, and miR-214-5p was identified as a regulator of TSG-6 mRNA.
Conclusion: Following a treatment with TNF α , ADSCs can regulate the inflammatory response in LPS-activated BV2 microglia by upregulating TSG-6 expression, which itself is under the negative control of miR-214-5p.
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