Open Access

ARTICLE

Substrate Modulation of Osteoblast Adhesion Strength, Focal Adhesion Kinase Activation, and Responsiveness to Mechanical Stimuli

E. Takai¹, R. Landesberg², R.W. Katz², C.T. Hung³, X.E Guo^1,4

1 Bone Bioengineering Laboratory, Department of Biomedical Engineering, Columbia University, New York, NY 10027
2 Cellular Engineering Laboratory, Department of Biomedical Engineering, Columbia University, New York, NY 10027
3 School of Dental and Oral Surgery, Columbia University, New York, NY, 10032.
4 Corresponding author, email: ed.guo@columbia.edu

Molecular & Cellular Biomechanics 2006, 3(1), 1-12. https://doi.org/10.3970/mcb.2006.003.001

Abstract

Osteoblast interactions with extracellular matrix (ECM) proteins are known to influence many cell functions, which may ultimately affect osseointegration of implants with the host bone tissue. Some adhesion-mediated events include activation of focal adhesion kinase, and subsequent changes in the cytoskeleton and cell morphology, which may lead to changes in adhesion strength and cell responsiveness to mechanical stimuli. In this study we examined focal adhesion kinase activation (FAK), F-actin cytoskeleton reorganization, adhesion strength, and osteoblast responsiveness to fluid shear when adhered to type I collagen (ColI), glass, poly-L-lysine (PLL), fibronectin (FN), vitronectin (VN), and serum (FBS). In general, surfaces that bind cells through integrins (FN, VN, FBS) elicited the highest adhesion strength, FAK activation, and F-actin stress fiber formation after both 15 and 60 minutes of adhesion. In contrast, cells attached through non-integrin mediated means (PLL, glass) showed the lowest FAK activation, adhesion strength, and little F-actin stress fiber formation. When subjected to steady fluid shear using a parallel plate flow chamber, osteoblasts plated on FN released significantly more prostaglandin E2 (PGE₂) compared to those on glass. In contrast, PGE₂ release of osteoblasts attached to FN or glass was not different in the absence of fluid shear, suggesting that differences in binding alone are insufficient to alter PGE₂ secretion. The increased adhesion strength as well as PGE₂ secretion of osteoblasts adhered via integrins may be due to increased F-actin fiber formation, which leads to increased cell stiffness.

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