Growth/differentiation factors (GDFs) play a significant role in numerous skeletal tissues and processes. Previous work using the brachypod mouse has suggested that GDF-5 affects Achilles tendon composition, ultrastructure, and material behavior, as well as tendon repair. The aim of the present stud
Effect of GDF-7 deficiency on tail tendon phenotype in mice
โ Scribed by Borjana Mikic; Rachel Entwistle; Kerri Rossmeier; LouAnn Bierwert
- Publisher
- Elsevier Science
- Year
- 2008
- Tongue
- English
- Weight
- 150 KB
- Volume
- 26
- Category
- Article
- ISSN
- 0736-0266
No coin nor oath required. For personal study only.
โฆ Synopsis
Abstract
The subfamily of growth/differentiation factors (GDFs) known as GDFs 5, 6, and 7 appears to be involved in tendon maintenance and repair, although the precise nature of this role has yet to be elucidated. The aim of the present study was to examine the role of GDFโ7 in tendon maintenance by studying tail tendon fascicle gene expression, composition, and material property strain rate dependency in 16โweekโold male and female GDFโ7 deficient mice. GDFโ7 deficiency did not affect the biochemical composition of tail tendon fascicles, nor did it significantly affect the tensile material properties obtained at either slow (5%/s) or fast (50%/s) strain rates. Further, no difference was found between genotypes in the strain rate sensitivity of any tensile material property. Consistent with the compositional analyses, QRTโPCR data did not reveal any differences of twofold or greater in the gene expression levels of collagens I, III, V, nor in the proteoglycans decorin, fibromodulin, lumican, biglycan, versican, or aggrecan. Gdf5 expression was upregulated twofold in GDFโ7 deficient tail tendons, and Bmp7 expression was downregulated twofold. No notable differences in expression levels for Bmp1โ6 or Gdf6 were detected. GDFโ5 protein levels were 50% higher in GDFโ7 deficient tail tendon compared to wild type tail tendon. The results of this study support the intriguing possibility that compensation by Gdfโ5 may be at least in part responsible for the absence of a strong phenotype in GDFโ7 deficient mice. ยฉ 2008 Orthopaedic Society. Published by Wiley Periodicals, Inc. J Orthop Res 26:834โ839, 2008
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