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Integrin display increases in the wounded rabbit medial collateral ligament but not the wounded anterior cruciate ligament

1995; Wiley; Volume: 13; Issue: 2 Linguagem: Inglês

10.1002/jor.1100130205

1554-527X

Paul J. Schreck, L. Kitabayashi, David Amiel, Wayne H. Akeson, Virgil L. Woods,

Cell Adhesion Molecules Research

Abstract 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 β 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 β 1 , α 5 , α 6 , and α v . Between 3 and 7 days, the wounded medial collateral ligament demonstrated a striking increase in staining for the β 1 , α 5 , and α v subunits on the fibroblasts, within the repair site, and on capillary endothelium. Increased staining was most marked for the β 1 subunit and less marked for the α 5 and α v subunits. The α 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. This study demonstrates that increased expression of integrins occurs coincident with wound healing in the medial collateral ligament, whereas this expression remains at baseline levels in the nonhealing wounded anterior cruciate ligament. This observation suggests that a failure to alter expression of integrins subsequent to injury may play a role in the defective healing of the anterior cruciate ligament.