MECHANICAL INJURY INCREASES BFGF AND CNTF MRMA EXPRESSION IN THE MOUSE RETINA

We characterized the survival-factor response of the normal mouse reti na to mechanical injury by examining the expression of mRNAs for basic fibroblast growth factor (bFGF), ciliary neurotrophic factor (CNTF), and their receptors, FGF receptor-1 (FGFR-1) and CNTF receptor alpha ( CNTFR-alpha). The retina was injured by making an incision through the choroid and retinal pigment epithelium that penetrated the subretinal space of each eye of an adult BALB/c mouse. Retinas were taken 6 hr, 12 hr, 1, 2, 4, 7, 10 and 16 days post-injury. Control animals were wi thout injury. Northern blot analysis was performed to determine bFGF, CNTF and their receptor mRNA levels. A significant increase in bFGF an d CNTF mRNAs was observed after injury, along with an increase in glia l fibrillary acidic protein (GFAP) expression. More than 2-fold of upr egulation of bFGF mRNA was seen as early as 6 hr after injury, This in crease reached a maximum of more than 5-fold at day 2 post-injury and then declined slowly, and was still about 2.5-fold of the control leve l by day 16. Expression of CNTF showed a small increase of about 1.6-f old at 6 hr after injury. The upregulation reached a peak level of abo ut 2.7-fold at day 4 after injury, then declined to control level by d ay 16. There was only a very small increase in FGFR-1 at 6, 12 and 24 hr after injury, and no significant increases in FGFR-1 at time points longer than 1 day post-injury. Expression of GFAP followed a time cou rse similar to that of bFGF. We conclude that mechanical injury induce s bFGF, CNTF, and GFAP expression in the mouse retina with time course s similar to the upregulation of these molecules in rat retina. Compar ed to the upregulation in rat retina, however, the injury-induced upre gulation of bFGF and GFAP is much less in the mouse retina. In additio n, there was only a very small induction of FGFR-1 expression in the m ouse retina, These Endings may explain, at least in part, the lack of injury-induced photoreceptor protection in the mouse retina. (C) 1997 Academic Press Limited.