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Regulatory role of collagen V in establishing mechanical properties of tendons and ligaments is tissue dependent.

Abstract
Patients with classic (type I) Ehlers-Danlos syndrome (EDS), characterized by heterozygous mutations in the Col5a1 and Col5a2 genes, exhibit connective tissue hyperelasticity and recurrent joint dislocations, indicating a potential regulatory role for collagen V in joint stabilizing soft tissues. This study asked whether the contribution of collagen V to the establishment of mechanical properties is tissue dependent. We mechanically tested four different tissues from wild type and targeted collagen V-null mice: the flexor digitorum longus (FDL) tendon, Achilles tendon (ACH), the anterior cruciate ligament (ACL), and the supraspinatus tendon (SST). Area was significantly reduced in the Col5a1(ΔTen/ΔTen) group in the FDL, ACH, and SST. Maximum load and stiffness were reduced in the Col5a1(ΔTen/ΔTen) group for all tissues. However, insertion site and midsubstance modulus were reduced only for the ACL and SST. This study provides evidence that the regulatory role of collagen V in extracellular matrix assembly is tissue dependent and that joint instability in classic EDS may be caused in part by insufficient mechanical properties of the tendons and ligaments surrounding each joint.
AuthorsBrianne K Connizzo, Benjamin R Freedman, Joanna H Fried, Mei Sun, David E Birk, Louis J Soslowsky
JournalJournal of orthopaedic research : official publication of the Orthopaedic Research Society (J Orthop Res) Vol. 33 Issue 6 Pg. 882-8 (Jun 2015) ISSN: 1554-527X [Electronic] United States
PMID25876927 (Publication Type: Comparative Study, Journal Article, Research Support, N.I.H., Extramural, Research Support, U.S. Gov't, Non-P.H.S.)
Copyright© 2015 Orthopaedic Research Society. Published by Wiley Periodicals, Inc.
Chemical References
  • Collagen Type V
Topics
  • Achilles Tendon (physiology)
  • Animals
  • Anterior Cruciate Ligament (physiology)
  • Biomechanical Phenomena
  • Collagen Type V (physiology)
  • Male
  • Mice, Transgenic

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