Literature DB >> 19279223

In vitro model to study chondrogenic differentiation in tendinopathy.

Marieke de Mos1, Wendy Koevoet, Hans T M van Schie, Nicole Kops, Holger Jahr, Jan A N Verhaar, Gerjo J V M van Osch.   

Abstract

BACKGROUND: Treatment of midportion Achilles tendinopathy is hampered by limited knowledge of the pathophysiology. HYPOTHESIS: Chondrogenic differentiation of tendon cells might take place in midportion Achilles tendinopathy and could be used as a target for drug treatment. An in vitro model for chondrogenic differentiation would be useful to evaluate existing and future treatment opportunities. STUDY: A controlled laboratory study.
METHODS: Perioperatively harvested tissue from human midportion Achilles tendinotic lesions and healthy Achilles tendons was analyzed by microscopy and real-time reverse transcription polymerase chain reaction. In vitro chondrogenic differentiation of tendon explants was induced using transforming-growth-factor beta. This model was modulated by removing the chondrogenic stimulus or adding triamcinolone or platelet-rich plasma.
RESULTS: Midportion Achilles tendinotic lesions had increased glycosaminoglycan staining and more rounded cell nuclei. Chondrogenic markers (sex-determining region Y)-box9, aggrecan, collagen 2, and RUNT-related transcription factor 2 were upregulated, but collagen 10 was not. Nondegenerative tendon explants cultured on chondrogenic medium had higher expression of aggrecan, collagen 2, and collagen 10 but not (sex-determining region Y)-box9 and RUNT-related transcription factor 2. Removing the chondrogenic stimulus decreased expression of aggrecan, collagen 2, and collagen 10. Both triamcinolone and platelet-rich plasma influenced the chondrogenic gene expression pattern in the in vitro model.
CONCLUSION: Chondrogenic differentiation is present in midportion Achilles tendinopathy. An in vitro model to study this chondrogenic differentiation was developed. CLINICAL RELEVANCE: This model can be used to investigate chondrogenic differentiation as a possible target for drug treatment, contributing to the development of more successful mechanism-based treatment opportunities.

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Year:  2009        PMID: 19279223     DOI: 10.1177/0363546508331137

Source DB:  PubMed          Journal:  Am J Sports Med        ISSN: 0363-5465            Impact factor:   6.202


  26 in total

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3.  Arguments for an increasing differentiation towards fibrocartilaginous components in midportion Achilles tendinopathy.

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4.  Fatigue loading of tendon results in collagen kinking and denaturation but does not change local tissue mechanics.

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5.  Mechanical changes in the Achilles tendon due to insertional Achilles tendinopathy.

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6.  Altered fate of tendon-derived stem cells isolated from a failed tendon-healing animal model of tendinopathy.

Authors:  Yun Feng Rui; Pauline Po Yee Lui; Yin Mei Wong; Qi Tan; Kai Ming Chan
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Review 7.  Current opinions on tendinopathy.

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8.  Genome-wide analysis identifies differential promoter methylation of Leprel2, Foxf1, Mmp25, Igfbp6, and Peg12 in murine tendinopathy.

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9.  Collagen type I and decorin expression in tenocytes depend on the cell isolation method.

Authors:  Markus U Wagenhäuser; Matthias F Pietschmann; Birte Sievers; Denitsa Docheva; Matthias Schieker; Volkmar Jansson; Peter E Müller
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10.  Extracorporeal Shock Wave Treatment (ESWT) improves in vitro functional activities of ruptured human tendon-derived tenocytes.

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