Molecular mediators of alphavbeta3-induced endothelial cell survival.

The alphavbeta3 integrin interaction with the extracellular matrix (ECM) plays an essential role in inhibiting apoptosis in endothelial cells. We have recently shown that alphavbeta3 ligation on rat aortic endothelial cells (RAECs) specifically activates the transcription factor nuclear factor kappaB (NF-kappaB) and promotes cell survival. Inhibiting NF-kappaB nuclear translocation abolished the protective effect of alphavbeta3 ligands.

Src kinase activity is required for integrin alphaVbeta3-mediated activation of nuclear factor-kappaB.

Integrin adhesion to extracellular matrix proteins protects adhesion-dependent cells from suspension-induced apoptosis. Previous studies indicate that activation of the transcription factor nuclear factor-kappaB was necessary for the integrin alpha(v)beta3 ligand osteopontin to protect endothelial cells from apoptosis caused by serum withdrawal. In this study, beta3 integrins were overexpressed in smooth muscle cells.

Differential effects of growth factors on tissue-engineered cartilage.

The effects of four regulatory factors on tissue-engineered cartilage were examined with specific focus on the ability to increase construct growth rate and concentrations of glycosaminoglycans (GAG) and collagen, the major extracellular matrix (ECM) components. Bovine calf articular chondrocytes were seeded onto biodegradable polyglycolic acid (PGA) scaffolds and cultured in medium with or without supplemental insulin-like growth factor (IGF-I), interleukin-4 (IL-4), transforming growth factor-beta1 (TGF-beta1) or platelet-derived growth factor (PDGF). IGF-I, IL-4, and TGF-beta1 increased construct wet weights by 1.