Wake Forest Institute for Regenerative Medicine, Wake Forest School of Medicine, Winston-Salem, NC 27157, USA.
Biomaterials. 2011 Oct;32(30):7555-61. doi: 10.1016/j.biomaterials.2011.06.061. Epub 2011 Jul 23.
Keratin biomaterials support cellular adhesion, proliferation and migration, which have led to their exploitation in a variety of biomedical applications. The mechanism of cell adhesion to keratin biomaterials, however, is poorly understood. Therefore, the goal of this work was to investigate the mechanisms by which human hair keratin-based biomaterials facilitate cellular adhesion. Hepatocytes were used as a model cell type due to the abundance of published data on cell adhesion mechanisms and their relatively copious attachment to keratin substrates. The roles of β(1)- and β(2)-integrins and the hepatic asialoglycoprotein receptor (ASGPR) in hepatocyte adhesion to keratin substrates were studied using attachment assays with and without function blocking antibodies. Blocking of the hepatic integrin subunits did not decrease hepatocyte attachment to keratin. Furthermore, adhesion to keratin did not result in the formation of focal complexes or focal adhesions, nor did it produce an upregulation of phosphorylated-focal adhesion kinase. However, inhibition of hepatic ASGPR decreased the ability of hepatocytes to attach to keratin substrates, which is indicative of the role of this glycoprotein receptor in hepatocyte binding to keratin biomaterials.
角蛋白生物材料支持细胞黏附、增殖和迁移，这使得它们在各种生物医学应用中得到了广泛的开发。然而，细胞黏附到角蛋白生物材料的机制还了解甚少。因此，这项工作的目的是研究人发角蛋白基生物材料促进细胞黏附的机制。由于已有大量关于细胞黏附机制及其相对丰富的黏附到角蛋白基质的研究数据，因此选择肝细胞作为模型细胞类型。使用带有和不带有功能阻断抗体的黏附测定法，研究了 β(1)-和 β(2)-整联蛋白以及肝唾液酸糖蛋白受体 (ASGPR) 在肝细胞黏附到角蛋白底物中的作用。阻断肝整合素亚基并没有降低肝细胞黏附到角蛋白。此外，黏附到角蛋白不会导致形成粘着斑或粘着点，也不会导致磷酸化粘着斑激酶的上调。然而，肝 ASGPR 的抑制降低了肝细胞附着到角蛋白底物的能力，这表明该糖蛋白受体在肝细胞与角蛋白生物材料结合中起作用。
