Neural cell adhesion molecule regulates chondrocyte hypertrophy in chondrogenic differentiation and experimental osteoarthritis.


Journal

Stem cells translational medicine
ISSN: 2157-6580
Titre abrégé: Stem Cells Transl Med
Pays: England
ID NLM: 101578022

Informations de publication

Date de publication:
02 2020
Historique:
received: 01 07 2019
accepted: 25 10 2019
pubmed: 20 11 2019
medline: 22 7 2021
entrez: 20 11 2019
Statut: ppublish

Résumé

Chondrocyte hypertrophy-like change is an important pathological process of osteoarthritis (OA), but the mechanism remains largely unknown. Neural cell adhesion molecule (NCAM) is highly expressed and involved in the chondrocyte differentiation of mesenchymal stem cells (MSCs). In this study, we found that NCAM deficiency accelerates chondrocyte hypertrophy in articular cartilage and growth plate of OA mice. NCAM deficiency leads to hypertrophic chondrocyte differentiation in both murine MSCs and chondrogenic cells, in which extracellular signal-regulated kinase (ERK) signaling plays an important role. Moreover, NCAM expression is downregulated in an interleukin-1β-stimulated OA cellular model and monosodium iodoacetate-induced OA rats. Overexpression of NCAM substantially inhibits hypertrophic differentiation in the OA cellular model. In conclusion, NCAM could inhibit hypertrophic chondrocyte differentiation of MSCs by inhibiting ERK signaling and reduce chondrocyte hypertrophy in experimental OA model, suggesting the potential utility of NCAM as a novel therapeutic target for alleviating chondrocyte hypertrophy of OA.

Identifiants

pubmed: 31742919
doi: 10.1002/sctm.19-0190
pmc: PMC6988767
doi:

Substances chimiques

Neural Cell Adhesion Molecules 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

273-283

Informations de copyright

© 2019 The Authors. Stem Cells Translational Medicine published by Wiley Periodicals, Inc. on behalf of AlphaMed Press.

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Auteurs

Bin-Feng Cheng (BF)

School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

Jun-Jiang Lian (JJ)

School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.
Shanghai Key Laboratory of Signaling and Disease Research, Laboratory of Receptor-based Bio-medicine, Collaborative Innovation Center for Brain Science, School of Life Sciences and Technology, Tongji University, Shanghai, People's Republic of China.

Hai-Jie Yang (HJ)

School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

Lei Wang (L)

School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

Hao-Heng Yu (HH)

Henan Key Laboratory of Medical Tissue Regeneration, School of Basic Medical Sciences, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

Jia-Jia Bi (JJ)

School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

Yao-Xin Gao (YX)

School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

Su-Juan Chen (SJ)

School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

Mian Wang (M)

School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

Zhi-Wei Feng (ZW)

School of Life Sciences and Technology, Xinxiang Medical University, Xinxiang, Henan, People's Republic of China.

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