Integrin display increases in the wounded rabbit medial collateral ligament but not the wounded anterior cruciate ligament.
The differential capacities of the anterior cruciate and medial collateral ligaments to heal may be related to differences in cellular function. This study tested the hypothesis that differential expression of integrins occurs in these ligaments after injury. The integrins are a family of cell surface receptors that mediate adhesion, migration, and other cellular functions critical to the healing of a wound. A similar complement and amount of the beta 1 subfamily of integrins are known to be present on the unperturbed anterior cruciate and medial collateral ligaments in humans and rabbits. A partial laceration was surgically created in these two ligaments in 12 anesthetized New Zealand White rabbits. Immunohistochemistry was performed on sections from the ligaments at 1, 3, 7, and 10 days after injury, using monoclonal antibodies directed against the integrin subunits beta 1, alpha 5, alpha 6, and alpha v. Between 3 and 7 days, the wounded medial collateral ligament demonstrated a striking increase in staining for the beta 1, alpha 5, and alpha v subunits on the fibroblasts, within the repair site, and on capillary endothelium. Increased staining was most marked for the beta 1 subunit and less marked for the alpha 5 and alpha v subunits. The alpha 6 subunit stained exclusively vascular structures within the healing medial collateral ligament. In marked contrast, the anterior cruciate ligament, which does not mount an effective repair response, demonstrated no comparable alteration of integrin expression from baseline levels.(ABSTRACT TRUNCATED AT 250 WORDS)[1]References
- Integrin display increases in the wounded rabbit medial collateral ligament but not the wounded anterior cruciate ligament. Schreck, P.J., Kitabayashi, L.R., Amiel, D., Akeson, W.H., Woods, V.L. J. Orthop. Res. (1995) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
