The study investigates the role of the extracellular matrix (ECM) as a cell survival factor, focusing on programmed cell death (PCD) or apoptosis. The researchers found that human endothelial cells rapidly undergo PCD when deprived of ECM interactions, characterized by cell morphology changes, nuclear fragmentation, DNA degradation, protein cross-linking, and the expression of the PCD-specific gene TRPM-2. PCD was blocked by plating cells on an immobilized integrin β1 antibody but not by antibodies to HLA or VCAM-1, suggesting that integrin-mediated signals are crucial for maintaining cell viability. Treatment with the tyrosine phosphatase inhibitor sodium orthovanadate also blocked PCD. The study further examines the role of ECM in other cell types, finding that some, but not all, cell types undergo rapid cell death when deprived of adhesion to the ECM. These findings suggest that the ECM functions as a survival factor for many cell types, regulating cell growth, differentiation, and behavior through integrin-mediated signaling.The study investigates the role of the extracellular matrix (ECM) as a cell survival factor, focusing on programmed cell death (PCD) or apoptosis. The researchers found that human endothelial cells rapidly undergo PCD when deprived of ECM interactions, characterized by cell morphology changes, nuclear fragmentation, DNA degradation, protein cross-linking, and the expression of the PCD-specific gene TRPM-2. PCD was blocked by plating cells on an immobilized integrin β1 antibody but not by antibodies to HLA or VCAM-1, suggesting that integrin-mediated signals are crucial for maintaining cell viability. Treatment with the tyrosine phosphatase inhibitor sodium orthovanadate also blocked PCD. The study further examines the role of ECM in other cell types, finding that some, but not all, cell types undergo rapid cell death when deprived of adhesion to the ECM. These findings suggest that the ECM functions as a survival factor for many cell types, regulating cell growth, differentiation, and behavior through integrin-mediated signaling.