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Activin suppresses the expression of inflammatory genes and signaling proteins in human leukemia monocytic THP-1 cells
被引:1
|作者:
Yun, Sang Oh
[1
]
Kim, Young Il
[2
]
Ahn, Hyung Joo
[1
]
Min, Sun Young
机构:
[1] Kyung Hee Univ, Coll Med, Kyung Hee Univ Hosp, Dept Surg, Seoul 02447, South Korea
[2] Kyung Hee Univ, Med Ctr, Med Sci Res Inst, Seoul 02447, South Korea
关键词:
THP-1;
cells;
activin A;
cytokine;
toll-like receptor;
matrix metal-lo-proteinase;
mitogen-activated protein kinase;
BINDING-PROTEIN;
FOLLISTATIN;
SECRETION;
RECEPTOR;
D O I:
10.14715/cmb/2023.69.11.6
中图分类号:
Q5 [生物化学];
Q7 [分子生物学];
学科分类号:
071010 ;
081704 ;
摘要:
Activin regulates inflammation, cell proliferation, immune response, wound repair, and endocrine function. In this study, we investigated the effect of activin on inflammatory genes in THP-1 cells and the involvement of NF-KB, AKT, and mitogen-activated protein kinase (MAPK) signaling. Cell viability was determined using a colorimetric assay with the MTS/PES solution. The mRNA levels were analyzed using reverse transcription quantitative polymerase chain reaction. The expression of NF-KB, AKT, and MAPK signaling proteins was measured using immunoblot analysis. Activin A did not affect THP-1 cell viability at concentrations below 50 ng/ml. Activin decreased the mRNA expression of cytokines (interleukin (IL)-1 beta, IL-6, and tumor necrosis factor-alpha (TNF-alpha), toll-like receptor 4 (TLR4), and matrix metallo-proteinases (MMP)-9 proteins but did not affect IL-8 expression. Activin increased the expression of TLR2 and MMP-2. In addition, activin inhibited the phosphorylation of NF-KB p65, AKT, and MAPK (c-Jun N-terminal kinase (JNK), extracellular signal -regulated kinase (ERK), and p38 MAPK) signaling proteins. Our results suggest that activin may be involved in anti inflammation by inhibiting inflammatory gene expression and regulating NF-KB and AKT/MAPK signaling.Copyright: (c) 2023 by the C.M.B. Association. All rights reserved
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页码:36 / 40
页数:5
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