The effect of mechanical load on integrin subunits α5 and β1 in chondrocytes from mature and immature cartilage explants

被引:56
作者
Lucchinetti, E
Bhargava, MM
Torzilli, PA
机构
[1] Hosp Special Surg, Lab Soft Tissue Res, New York, NY 10021 USA
[2] Univ Zurich, Inst Pharmacol & Toxicol, Sect Cardiovasc Res, CH-8057 Zurich, Switzerland
关键词
chondrocytes; cartilage; mechanotransduction; integrins; tissue culture (bovine);
D O I
10.1007/s00441-003-0836-8
中图分类号
Q2 [细胞生物学];
学科分类号
071009 [细胞生物学]; 090102 [作物遗传育种];
摘要
Articular cartilage is subjected to cyclic compressive stresses during joint loading. There is increasing experimental evidence that this loading is essential for the chondrocytes to maintain the functionality of the cartilage extracellular matrix (ECM) and that members of the integrin family of transmembrane receptors may play an important role in signal mechanotransduction between the ECM and chondrocytes. Of particular interest are the integrin subunits alpha5 and beta1, which are known to form the receptor for fibronectin, an important ECM protein, and to be involved in mechanotransduction as well as in the regulation of cytokine production. In this study, we measured the amounts of the integrin subunits alpha5 and beta1 in chondrocytes from young (immature) and adult (mature) bovine articular cartilage explants which were subjected to a continuously applied cyclic compressive stress of 1 MPa for 6 and 24 h. The integrin content per chondrocyte was measured immediately after load cessation by flow cytometry following matrix digestion to release the cells. We found that a mechanical stress induced an increase in the number of integrin subunit alpha5 in immature and mature cartilage but not in the integrin subunit beta1 content. The integrin contents were greatest after 6 h of loading and returned to control levels after 24 h of unloading. The results of this study supply further experimental evidence that chondrocytes respond to changes in their mechanical environment and that the integrin alpha5beta1 may act as a mechanical signal transducer between the chondrocyte and the ECM for the modulation of cellular physiology.
引用
收藏
页码:385 / 391
页数:7
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