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A Comparison of Type I Collagen, Fibronectin, and Vitronectin in Supporting Adhesion of Mechanically Strained Osteoblasts
Author(s) -
Lacouture Mario E.,
Schaffer Jonathan L.,
Klickstein Lloyd B.
Publication year - 2002
Publication title -
journal of bone and mineral research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.882
H-Index - 241
eISSN - 1523-4681
pISSN - 0884-0431
DOI - 10.1359/jbmr.2002.17.3.481
Subject(s) - vitronectin , fibronectin , integrin , osteopontin , microbiology and biotechnology , type i collagen , cell adhesion , strain (injury) , adhesion , chemistry , receptor , biology , cell , immunology , biochemistry , extracellular matrix , anatomy , endocrinology , organic chemistry
We used an adhesion assay for cells cultured under high dynamic strain to measure human osteoblast‐like HOS cell adherence to immobilized type I collagen, fibronectin, and vitronectin. These conditions were designed to model the increased forces present at unstable fractures or loose joint prostheses. At a constant, low protein‐coating density (1000 molecules/μm 2 ) and 20% cyclic strain for 24 h, type I collagen, fibronectin, and vitronectin supported 24.6 ± 2%, 16.7 ± 3%, and 1.1 ± 1% adherence, respectively, which paralleled the relative number of integrin‐binding sites in each protein. Thus, when the number of available binding sites was limited, strain resistance was proportional to the number of integrin‐ligand interactions. In contrast, at high protein‐coating densities (≥2,500 molecules/μm 2 ), vitronectin supported greater adherence (45.7 ± 2%) when compared with type I collagen (37 ± 2%) or fibronectin (34.8 ± 2%) and directed constitutive expression of osteopontin (OPN), which suggested that there exist discrete signals on vitronectin receptor occupancy that promoted cell adherence and survival under strain. Integrin‐mediated binding was necessary for resistance to strain, as evidenced by the low levels of strain resistance observed when cells were adherent in a nonintegrin‐dependent manner. These findings support the utilization of at least two distinct mechanisms (i.e., tensegrity and integrin‐mediated signal transduction) by HOS cells to remain adherent and viable on exposure to mechanical forces.