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Regulation of gene expression in human tendinopathy.


ABSTRACT: BACKGROUND: Chronic tendon injuries, also known as tendinopathies, are common among professional and recreational athletes. These injuries result in a significant amount of morbidity and health care expenditure, yet little is known about the molecular mechanisms leading to tendinopathy. METHODS: We have used histological evaluation and molecular profiling to determine gene expression changes in 23 human patients undergoing surgical procedures for the treatment of chronic tendinopathy. RESULTS: Diseased tendons exhibit altered extracellular matrix, fiber disorientation, increased cellular content and vasculature, and the absence of inflammatory cells. Global gene expression profiling identified 983 transcripts with significantly different expression patterns in the diseased tendons. Global pathway analysis further suggested altered expression of extracellular matrix proteins and the lack of an appreciable inflammatory response. CONCLUSIONS: Identification of the pathways and genes that are differentially regulated in tendinopathy samples will contribute to our understanding of the disease and the development of novel therapeutics.

SUBMITTER: Jelinsky SA 

PROVIDER: S-EPMC3095578 | biostudies-literature | 2011

REPOSITORIES: biostudies-literature

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Regulation of gene expression in human tendinopathy.

Jelinsky Scott A SA   Rodeo Scott A SA   Li Jian J   Gulotta Lawrence V LV   Archambault Joanne M JM   Seeherman Howard J HJ  

BMC musculoskeletal disorders 20110503


<h4>Background</h4>Chronic tendon injuries, also known as tendinopathies, are common among professional and recreational athletes. These injuries result in a significant amount of morbidity and health care expenditure, yet little is known about the molecular mechanisms leading to tendinopathy.<h4>Methods</h4>We have used histological evaluation and molecular profiling to determine gene expression changes in 23 human patients undergoing surgical procedures for the treatment of chronic tendinopath  ...[more]

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