Objective:
Vascular endothelial growth factor (VEGF) expression promotes angiogenesis and neuronal
repair. The aim of this study was to investigate VEGF expression in relation to neurodegeneration,
either caused by hyperoxia, a frequent problem in the treatment of preterm infants
with respiratory dysfunction, or caused by brain injury, an important complication
(e.g. in case of intracerebral haemorrhage) in the early neonatal period of immature
newborns.
Methods:
6 d old Wistar rat pups were either subjected to 80% oxygen or treated with phorbolester.
After 0, 2, 6, 12 and 24h of exposition animals (n = 5 per group) were sacrificed
and the brain cortices were processed for molecular experiments on RNA (quantitative
RT-PCR) and protein (Western blot) levels using VEGF specific primers and antibodies.
Results:
In association with hyperoxia a decrease in VEGF mRNA expression down to about 25%
of the basal level of the control animals (no additional oxygen exposition) was noted.
This effect was already evident at 2h with a minimum of VEGF mRNA expression at 2h
and 6h (p < 0.01). The protein expression also showed a decrease of VEGF signal associated
with hyperoxia. The weakest signal appeared at 12h (p < 0.01). In the case of phorbolester
treatment we have seen an increase of VEGF expression up to about 200% compared to
the controls, with a maximum of mRNA at 6h (p < 0.01) and a maximum of protein expression
at 12h and 24h (p < 0.05).
Conclusion:
Exposure of newborn rats to hyperoxia induces a statistically significant time-dependent
decrease, treatment with phorbolester a statistically significant time-dependent increase
in VEGF expression in the cortices of the animals. These effects are evident on the
transcriptional and translational level.
