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Creating an animal model of tendinopathy by inducing chondrogenic differentiation with kartogenin

Yuan, T and Zhang, J and Zhao, G and Zhou, Y and Zhang, CQ and Wang, JHC (2016) Creating an animal model of tendinopathy by inducing chondrogenic differentiation with kartogenin. PLoS ONE, 11 (2).

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Abstract

© 2016 Yuan et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Previous animal studies have shown that long term rat treadmill running induces over-use tendinopathy, which manifests as proteoglycan accumulation and chondrocytes-like cells within the affected tendons. Creating this animal model of tendinopathy by long term treadmill running is however time-consuming, costly and may vary among animals. In this study, we used a new approach to develop an animal model of tendinopathy using kartogenin (KGN), a bio-compound that can stimulate endogenous stem/progenitor cells to differentiate into chondrocytes. KGN-beads were fabricated and implanted into rat Achilles tendons. Five weeks after implantation, chondrocytes and proteoglycan accumulation were found at the KGN implanted site. Vascularity as well as disorganization in collagen fibers were also present in the same site along with increased expression of the chondrocyte specific marker, collagen type II (Col. II). In vitro studies confirmed that KGN was released continuously from KGN-alginate in vivo beads and induced chondrogenic differentiation of tendon stem/progenitor cells (TSCs) suggesting that chondrogenesis after KGN-bead implantation into the rat tendons is likely due to the aberrant differentiation of TSCs into chondrocytes. Taken together, our results showed that KGN-alginate beads can be used to create a rat model of tendinopathy, which, at least in part, reproduces the features of over-use tendinopathy model created by long term treadmill running. This model is mechanistic (stem cell differentiation), highly reproducible and precise in creating localized tendinopathic lesions. It is expected that this model will be useful to evaluate the effects of various topical treatments such as NSAIDs and platelet-rich plasma (PRP) for the treatment of tendinopathy. Copyright:


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Details

Item Type: Article
Status: Published
Creators/Authors:
CreatorsEmailPitt UsernameORCID
Yuan, T
Zhang, Jjianying@pitt.eduJIANYING
Zhao, G
Zhou, Y
Zhang, CQ
Wang, JHCwanghc@pitt.eduWANGHC
Contributors:
ContributionContributors NameEmailPitt UsernameORCID
EditorDong, YufengUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Date: 1 February 2016
Date Type: Publication
Access Restriction: No restriction; Release the ETD for access worldwide immediately.
Journal or Publication Title: PLoS ONE
Volume: 11
Number: 2
DOI or Unique Handle: 10.1371/journal.pone.0148557
Institution: University of Pittsburgh
Schools and Programs: School of Medicine > Orthopaedic Surgery
Refereed: Yes
Date Deposited: 23 Aug 2016 15:07
Last Modified: 02 Feb 2019 16:56
URI: http://d-scholarship.pitt.edu/id/eprint/28314

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