In Vitro Model to Study Chondrogenic Differentiation in Tendinopathy

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

doi:10.1177/0363546508331137

Cited by 71 publications

(76 citation statements)

References 39 publications

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“…Increases were noted in the concentrations of PDGF, VEGF, TGF␤, and hepatocyte growth factor (HGF), four growth factors that promote matrix production. A 2008 report indicated that tenocyte proliferation increased when human hamstring tendon fragments were cultured in PRP [20,21]. In another study of human hamstring tendon, PRP increased fibroblast proliferation and VEGF expression by tenocytes [22].…”

Section: Prp Effects On Human Cells and Tendonsmentioning

confidence: 99%

Does platelet-rich plasma deserve a role in the treatment of tendinopathy?

et al. 2015

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Section: Prp Effects On Human Cells and Tendonsmentioning

confidence: 99%

Does platelet-rich plasma deserve a role in the treatment of tendinopathy?

et al. 2015

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“…Tendon injuries represent a significant clinical problem, and details of the pathological changes in overloaded tendon and the associated development of tendinopathy are sparse (Arnoczky et al, 2007). Focal histopathological changes have been documented in the region of the overused tendon, including collagen disorganization, increased cellularity, cell rounding and neovascularisation (de Mos et al, 2009). Further it has been shown that expression of both collagen type I, collagen type III, matrix metalloproteinases and other ECM proteins is higher in tendinopathic than in healthy tendon (de Mos et al, 2007, Jones et al, 2006) and that the tissue content of several proteins like versican and aggrecan is upregulated in tendinopathy (Parkinson et al, 2010).…”

Section: Introductionmentioning

confidence: 99%

3‐D ultrastructure and collagen composition of healthy and overloaded human tendon: evidence of tenocyte and matrix buckling

et al. 2014

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Achilles tendinopathies display focal tissue thickening with pain and ultrasonography changes. Whilst complete rupture might be expected to induce changes in tissue organization and protein composition, little is known about the consequences of non-rupture-associated tendinopathies, especially with regards to changes in the content of collagen type I and III (the major collagens in tendon) and changes in tendon fibroblast (tenocyte) shape and organization of the extracellular matrix. To gain new insights, we took biopsies from the tendinopathic region and flanking healthy region of Achilles tendons of six individuals with clinically diagnosed tendinopathy who had no evidence of cholesterol, uric acid and amyloid accumulation. Biochemical analysis of collagen III/I ratio were performed on all six individuals and electron microscope analysis using transmission electron microscopy and serial block face-scanning electron microscopy were made on two individuals. In the tendinopathic regions, compared to the flanking healthy tissue, we observed 1) an increase in the ratio of collagen III:I proteins, 2) buckling of the collagen fascicles in the extracellular matrix, 3) buckling of tenocytes and their nuclei, and 4) an increase in the ratio small:large diameter collagen fibrils. In summary, load-induced non-rupture tendinopathy in humans is associated with localized biochemical changes, a shift from large to small diameter fibrils, buckling of the tendon extracellular matrix, and buckling of the cells and their nuclei.

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“…Chondroid metaplasia has been histologically identified in tissue biopsies of Achilles tendinopathy in humans [16]. A few studies have raised the possibility that native tendon cells may be able to undergo chondrogenic differentiation, and there is evidence for load-dependent regulation of cartilaginous phenotypes within the tendon [17], [18]. Despite the cellular origin or mechanical contribution to the chondroid heterogeneity, the presence of this tendinopathic marker validates degenerative tissue changes in the aged rat model used in this study.…”

Section: Resultssupporting

confidence: 56%

Metabolic Divergence of Aged Tenocytes: Insights into Tendinopathic Disease Progression

Patterson

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ii iii Acknowledgements:This project was only possible due to the support and hard work of many people, who have played a pivotal role in my research project over the last 2 years. I am sincerely grateful and it was truly an honor to work with you.First, I must thank Dr. Joseph Park, my advisor and the principal investigator of this project. Dr. Park was confident in my abilities as a researcher and student since the first day I stepped into his office. He provided me with an opportunity that made my graduate experience possible. He then continued to provide guidance, vision, and encouragement to drive this project forward.To my thesis committee consisting of Dr. Shayn Peirce-Cottler, Dr. Gary Balian, and Dr. Zhen Yan, I am grateful for your guidance and critique that was essential to questioning my hypothesis, developing new insights, and strengthening my research as a whole.To Dr. Ching-Hua Yeh, I could not ask for a more committed mentor. I am thankful for your guidance in the lab. I simply would not have been able to accomplish this work without your help.To Dr. Shaharyar Khan, Dr. Francisco Portel, Dr. Jameel Dennis, and Dr. Isaac Onyango, thank you for your time and energy teaching me in the lab. Our collaboration was a key inroad to establishing my project.To Dr. Kyle Hoehn and Brandon Kenwood, your experimental help was critical to completing my examination of cellular metabolism.To Dr. Abhijit Dighe, your research knowledge, experimental reasoning, and forthright criticism are truly unmatched in my eyes. You have greatly contributed to my work through your critique and enthusiasm, thank you.To Dr. Jan Redick and Dr. Stacy Guillot, your contributions and knowledge of advanced microscopy techniques was a great help to several aspects of my project.To Sheri VanHoose, I am grateful for your assistance in preparing my tissue histology work.To Gina Beck, thank you for helping me to get started in the lab. I appreciate your time and patience in the earliest days of my tenure with the orthopedics lab.iv To my lab members in the Department of Orthopedics, thank you for your advice, criticism, guidance, and patience that you kindly exhibited each and every day.To the Departments of Biomedical Engineering and Orthopedics, the academic community here at UVa is outstanding. The faculty, staff, and students have played an invaluable role in promoting my research experience at UVa.To my friends and family, I can never thank you enough for providing inspiration and support.v In this investigation, progression of tendinopathy was identified in Achilles tendon from aged, 22-month old, rats. Primary tendon cell cultures from the older rats were characterized and these culture systems were utilized in two subsequent studies detailing age-dependent dysfunction. In the first study, the aged cells were examined for fundamental changes in glycolytic and oxidative function to examine the possibility of an age-dependent basis correlating energy metabolism and the lack of tissue maintenance. Although there is no definitive evide...

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In Vitro Model to Study Chondrogenic Differentiation in Tendinopathy

Abstract: 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.

Cited by 71 publications

References 39 publications

Does platelet-rich plasma deserve a role in the treatment of tendinopathy?

Does platelet-rich plasma deserve a role in the treatment of tendinopathy?

3‐D ultrastructure and collagen composition of healthy and overloaded human tendon: evidence of tenocyte and matrix buckling

Metabolic Divergence of Aged Tenocytes: Insights into Tendinopathic Disease Progression

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