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The Regulatory Role of Signaling Crosstalk in Hypertrophy of MSCs and Human Articular Chondrocytes.
Int J Mol Sci. 2015 Aug 14; 16(8):19225-47.IJ

Abstract

Hypertrophic differentiation of chondrocytes is a main barrier in application of mesenchymal stem cells (MSCs) for cartilage repair. In addition, hypertrophy occurs occasionally in osteoarthritis (OA). Here we provide a comprehensive review on recent literature describing signal pathways in the hypertrophy of MSCs-derived in vitro differentiated chondrocytes and chondrocytes, with an emphasis on the crosstalk between these pathways. Insight into the exact regulation of hypertrophy by the signaling network is necessary for the efficient application of MSCs for articular cartilage repair and for developing novel strategies for curing OA. We focus on articles describing the role of the main signaling pathways in regulating chondrocyte hypertrophy-like changes. Most studies report hypertrophic differentiation in chondrogenesis of MSCs, in both human OA and experimental OA. Chondrocyte hypertrophy is not under the strict control of a single pathway but appears to be regulated by an intricately regulated network of multiple signaling pathways, such as WNT, Bone morphogenetic protein (BMP)/Transforming growth factor-β (TGFβ), Parathyroid hormone-related peptide (PTHrP), Indian hedgehog (IHH), Fibroblast growth factor (FGF), Insulin like growth factor (IGF) and Hypoxia-inducible factor (HIF). This comprehensive review describes how this intricate signaling network influences tissue-engineering applications of MSCs in articular cartilage (AC) repair, and improves understanding of the disease stages and cellular responses within an OA articular joint.

Authors+Show Affiliations

Developmental BioEngineering, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede 7500 AE, The Netherlands. l.zhong@utwente.nl.Developmental BioEngineering, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede 7500 AE, The Netherlands. xiaobinhuang@cqu.edu.cn. School of Life Sciences, Chongqing University, Chongqing 400030, China. xiaobinhuang@cqu.edu.cn.Developmental BioEngineering, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede 7500 AE, The Netherlands. h.b.j.karperien@utwente.nl.Developmental BioEngineering, MIRA Institute for Biomedical Technology and Technical Medicine, University of Twente, Enschede 7500 AE, The Netherlands. j.n.post@utwente.nl.

Pub Type(s)

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

Language

eng

PubMed ID

26287176

Citation

Zhong, Leilei, et al. "The Regulatory Role of Signaling Crosstalk in Hypertrophy of MSCs and Human Articular Chondrocytes." International Journal of Molecular Sciences, vol. 16, no. 8, 2015, pp. 19225-47.
Zhong L, Huang X, Karperien M, et al. The Regulatory Role of Signaling Crosstalk in Hypertrophy of MSCs and Human Articular Chondrocytes. Int J Mol Sci. 2015;16(8):19225-47.
Zhong, L., Huang, X., Karperien, M., & Post, J. N. (2015). The Regulatory Role of Signaling Crosstalk in Hypertrophy of MSCs and Human Articular Chondrocytes. International Journal of Molecular Sciences, 16(8), 19225-47. https://doi.org/10.3390/ijms160819225
Zhong L, et al. The Regulatory Role of Signaling Crosstalk in Hypertrophy of MSCs and Human Articular Chondrocytes. Int J Mol Sci. 2015 Aug 14;16(8):19225-47. PubMed PMID: 26287176.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - The Regulatory Role of Signaling Crosstalk in Hypertrophy of MSCs and Human Articular Chondrocytes. AU - Zhong,Leilei, AU - Huang,Xiaobin, AU - Karperien,Marcel, AU - Post,Janine N, Y1 - 2015/08/14/ PY - 2015/07/07/received PY - 2015/08/07/accepted PY - 2015/8/20/entrez PY - 2015/8/20/pubmed PY - 2016/5/25/medline KW - articular cartilage KW - chondrocytes KW - chondrogenesis KW - hypertrophy KW - mesenchymal stem cells KW - osteoarthritis KW - review KW - signal crosstalk KW - signaling SP - 19225 EP - 47 JF - International journal of molecular sciences JO - Int J Mol Sci VL - 16 IS - 8 N2 - Hypertrophic differentiation of chondrocytes is a main barrier in application of mesenchymal stem cells (MSCs) for cartilage repair. In addition, hypertrophy occurs occasionally in osteoarthritis (OA). Here we provide a comprehensive review on recent literature describing signal pathways in the hypertrophy of MSCs-derived in vitro differentiated chondrocytes and chondrocytes, with an emphasis on the crosstalk between these pathways. Insight into the exact regulation of hypertrophy by the signaling network is necessary for the efficient application of MSCs for articular cartilage repair and for developing novel strategies for curing OA. We focus on articles describing the role of the main signaling pathways in regulating chondrocyte hypertrophy-like changes. Most studies report hypertrophic differentiation in chondrogenesis of MSCs, in both human OA and experimental OA. Chondrocyte hypertrophy is not under the strict control of a single pathway but appears to be regulated by an intricately regulated network of multiple signaling pathways, such as WNT, Bone morphogenetic protein (BMP)/Transforming growth factor-β (TGFβ), Parathyroid hormone-related peptide (PTHrP), Indian hedgehog (IHH), Fibroblast growth factor (FGF), Insulin like growth factor (IGF) and Hypoxia-inducible factor (HIF). This comprehensive review describes how this intricate signaling network influences tissue-engineering applications of MSCs in articular cartilage (AC) repair, and improves understanding of the disease stages and cellular responses within an OA articular joint. SN - 1422-0067 UR - https://www.unboundmedicine.com/medline/citation/26287176/The_Regulatory_Role_of_Signaling_Crosstalk_in_Hypertrophy_of_MSCs_and_Human_Articular_Chondrocytes_ DB - PRIME DP - Unbound Medicine ER -