PURPOSE. To test the effects of osmotic change on basic fibroblast growth f
actor (bFGF) release from cultured endothelial cells (ECs).
METHODS. Bovine aortic and bovine retinal ECs were exposed to hypoosmotic s
hock for 2 minutes, were allowed to recover for 15 minutes, and had bFGF re
lease assayed. The role of bFGF in cell recovery was assessed by including
neutralizing antibody against bFGF or the addition of exogenous bFGF, Cell
number and viability were determined under varying conditions. Apoptosis wa
s assessed by immunoperoxidase detection of digoxigenin-labeled DNA.
RESULTS. After shock and recovery, both ECs released significantly greater
amounts of bFGF than untreated control. bFGF release after shock fur 2 minu
tes mas lower than release after shuck and recovery. Bovine retinal endothe
lial (BRE) cell number was reduced at 48 hours after shock, recovery, and r
emoval of released bFGF compared with cells left in the presence of release
d bFGF, Cell number was significantly lower when BRE cells were shocked and
recovered in the presence of a neutralizing anti-bFGF antibody (P < 0.05).
Exogenous bFGF reversed this effect. Apoptosis was significantly increased
in BRE cells shocked and recovered or in the presence of bFGF antibody (P
CONCLUSIONS. bFGF is released by cultured ECs in response to osmotically in
duced cell injury. These results support the concept of bFGF as a "wound" h
ormone and survival factor for ECs. in further compromised tissue, release
of bFGF in this manner mat play a role in the pathogenesis of disease.