Authors
Mingzheng Zhang, Laura C W Peeters, Pieter J Emans, Adhiambo M A Witlox, Guus G H van den Akker, Tim J M Welting, Marjolein M J Caron
Published in
Peptides. Pages 171521. Sep 23, 2026. Epub Sep 23, 2026.
Abstract
The BMP7-derived peptide p[63-82] improves a healthy chondrocyte phenotype and attenuates chondrocyte hypertrophy in human osteoarthritic chondrocytes. In cartilage regeneration strategies, chondrogenic differentiation of progenitor cells is often hampered by hypertrophic differentiation of the newly formed cartilaginous tissue. In this study, we explored the pro-chondrogenic and anti-hypertrophic effects of peptide p[63-82] in different progenitor-based chondrogenic differentiation models. Chondrogenic differentiation was induced in ATDC5 cells, human bone marrow-derived stem cells (hBMSCs), and rabbit periosteal progenitor cells (rPCs) in the absence or presence of peptide p[63-82]. In all models, increased gene expression of Sox9, Nkx3.2, Col2a1, Acan and GAG content was observed in the peptide p[63-82] condition, indicative of a pro-chondrogenic effect. Expression of hypertrophic genes Runx2, Col10a1, Alpl and Rmrp and ALP enzyme activity were prevented by the p[63-82] peptide-exposed cultures. Nkx3.2 signaling is, partly, responsible for the observed p[63-82] effects. The peptide p[63-82] was thus able to promote a chondrogenic phenotype, whilst preventing the development of chondrocyte hypertrophy in ATDC5 cells, hBMSCs and rPCs. The p[63-82] peptide could be a promising candidate for optimizing cell-based cartilage repair strategies after validation in in vivo models.
PMID:
42778025
Bibliographic data and abstract were imported from PubMed on 24 Sep 2026.
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