Macrophage migration inhibitory factor reversed senescent phenotype in human chondrocytes in vitro.

Chondrocytes Macrophage migration inhibitory factor Osteoarthritis Senescence

Journal

Molecular biology reports
ISSN: 1573-4978
Titre abrégé: Mol Biol Rep
Pays: Netherlands
ID NLM: 0403234

Informations de publication

Date de publication:
21 Jan 2024
Historique:
received: 26 09 2023
accepted: 04 12 2023
medline: 21 1 2024
pubmed: 21 1 2024
entrez: 21 1 2024
Statut: epublish

Résumé

The senescence of chondrocytes, which is closely linked to the development of osteoarthritis (OA), has been found to be influenced by the inflammatory environment of joint cavity. However, there remains a lack of comprehensive understanding regarding the specific mechanisms through which cytokine impacts chondrocytes senescence. To investigate the effects of MIF on the chondrocytes senescence and explore the underlying mechanism. Human cytokine array and ELISA were used for the level of MIF in synovium fluid. CCK-8 was used for chondrocytes viability. IF, WB, SA-β-gal staining and flow cytometry were used for the chondrogenic, apoptotic and senescent phenotype of chondrocytes. The level of MIF was significantly increased in OA patients. MIF significantly reversed the senescent phenotype induced by LPS pretreatment in human chondrocytes. MIF significantly enhanced the expression of Col II, SOX9, and ACAN in LPS pre-treated human chondrocytes. Furthermore, MIF significantly inhibited the apoptosis of LPS-induced senescent chondrocytes. Increased level of MIF in osteoarthritic joint cavity might effectively suppress the senescent phenotype and simultaneously improve the chondrogenic phenotype in chondrocytes, the underlying mechanism was likely to be independent of apoptosis.

Sections du résumé

BACKGROUND BACKGROUND
The senescence of chondrocytes, which is closely linked to the development of osteoarthritis (OA), has been found to be influenced by the inflammatory environment of joint cavity. However, there remains a lack of comprehensive understanding regarding the specific mechanisms through which cytokine impacts chondrocytes senescence.
PURPOSE OBJECTIVE
To investigate the effects of MIF on the chondrocytes senescence and explore the underlying mechanism.
METHODS METHODS
Human cytokine array and ELISA were used for the level of MIF in synovium fluid. CCK-8 was used for chondrocytes viability. IF, WB, SA-β-gal staining and flow cytometry were used for the chondrogenic, apoptotic and senescent phenotype of chondrocytes.
RESULTS RESULTS
The level of MIF was significantly increased in OA patients. MIF significantly reversed the senescent phenotype induced by LPS pretreatment in human chondrocytes. MIF significantly enhanced the expression of Col II, SOX9, and ACAN in LPS pre-treated human chondrocytes. Furthermore, MIF significantly inhibited the apoptosis of LPS-induced senescent chondrocytes.
CONCLUSION CONCLUSIONS
Increased level of MIF in osteoarthritic joint cavity might effectively suppress the senescent phenotype and simultaneously improve the chondrogenic phenotype in chondrocytes, the underlying mechanism was likely to be independent of apoptosis.

Identifiants

DOI: 10.1007/s11033-023-09101-0 PMID: 38245877
pubmed: 38245877
doi: 10.1007/s11033-023-09101-0
pii: 10.1007/s11033-023-09101-0
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

154

Subventions

Organisme : Chongqing Postdoctoral Research Project Special Fund
ID : 2021XM3033
Organisme : Chongqing Natural Science Foundation
ID : cstc2021jcyj-msxmX0135
Organisme : Chongqing Key Laboratory of Precision Medicine in Joint Surgery
ID : 425Z2138
Organisme : Chongqing Excellent Scientist Project
ID : 425Z2W21

Informations de copyright

© 2024. The Author(s), under exclusive licence to Springer Nature B.V.

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Auteurs

Zhenlan Fu (Z)

Center for Joint Surgery, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China.

Qingqing Li (Q)

Key Laboratory of Biorheological Science and Technology, Ministry of Education College of Bioengineering, Chongqing University, Chongqing, 400044, China.

Peiyao Jiang (P)

Center for Joint Surgery, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China.

Xiongbo Song (X)

Center for Joint Surgery, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China.

Junjun Yang (J)

Key Laboratory of Biorheological Science and Technology, Ministry of Education College of Bioengineering, Chongqing University, Chongqing, 400044, China.

Guangxing Chen (G)

Center for Joint Surgery, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China. cgx7676@hotmail.com.

Xiaoyuan Gong (X)

Center for Joint Surgery, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China. sliegxy@foxmail.com.

Liu Yang (L)

Center for Joint Surgery, Southwest Hospital, Army Medical University (Third Military Medical University), Chongqing, 400038, China. jointsurgery@163.com.

Classifications MeSH