Protection from Apoptosis of Endothelial Cells by Albumin

Apoptosis is programmed cell death and is thought to be responsible for the removal of excess cells in tissues (Gerschenson and Rotello, 1992). Endothelial cells are known to undergo apoptosis in-vivo (Walker etal, 1989; Walker and Gobe, 1987). Similarly, apoptosis has been observed in cultured HUVEC deprived of serum and or attachment (Araki et al., 1990; Araki et al., 1990; Meredith et al, 1993). We have found that bovine (BSA) and human (HSA) serum albumin both block the loss of attachment and DNA fragmentation typical of HUVEC apoptosis. There is no difference in the dose response of the two albumins in their ability to prevent loss of attachment, and the response is maximal at concentrations approaching those in blood. However, albumin is not able to rescue HUVEC after 8 hr of serum starvation, while before this time it is only partially effective in rescuing HUVEC. Serum on the other hand is able to rescue serum starved cells at all time points tested (up to 18 hr). This suggests that serum contains other factors blocking apoptosis such as fibroblast growth factor (Araki et al, 1990). BSA is partially inactivated by CNBr, while HSA is unaffected. Reduction of both albumins results in inactivation. We suggest that the effect of albumin in blocking apoptosis may provide a mechanism for the removal of nonfunctional vessels in-vivo.