Purchase this article with an account.
M. Elizabeth Hartnett, Claudia M. Garcia, Patricia A. D’Amore; Release of bFGF, an Endothelial Cell Survival Factor, by Osmotic Shock. Invest. Ophthalmol. Vis. Sci. 1999;40(12):2945-2951.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
purpose. To test the effects of osmotic change on basic fibroblast growth factor
(bFGF) release from cultured endothelial cells (ECs).
methods. Bovine aortic and bovine retinal ECs were exposed to hypoosmotic shock
for 2 minutes, were allowed to recover for 15 minutes, and had bFGF
release 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 was assessed by immunoperoxidase detection of
results. After shock and recovery, both ECs released significantly greater
amounts of bFGF than untreated control. bFGF release after shock for 2
minutes was lower than release after shock and recovery. Bovine retinal
endothelial (BRE) cell number was reduced at 48 hours after shock,
recovery, and removal of released bFGF compared with cells left in the
presence of released 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 < 0.001).
conclusions. bFGF is released by cultured ECs in response to osmotically induced
cell injury. These results support the concept of bFGF as a “wound”
hormone and survival factor for ECs. In further compromised tissue,
release of bFGF in this manner may play a role in the pathogenesis of
This PDF is available to Subscribers Only