Abstract
Purpose: :
In previous study, we confirmed that the retinas in oxygen-induced retinopathy (OIR) rats as an experimental model of retinopathy of prematurity at postnatal (P) 18 show most severe retinal neovascular pathology. We here investigated expression of Growth-associated pretein(GAP)-43 and phospho-GAP-43 in retina of OIR rats at P18. We also examined the effect of triamcinolone acetonide (TA), a corticosteroid, on the expression of GAP-43 and phospho-GAP-43
Methods: :
OIR was induced by exposure of hyperoxia to SD rats from P2 to P14 and then returned to normoxic conditions. TA was intravitreal-injected once into the right eye of OIR rats at P15. GAP-43 mRNA at P18 were determined by Reverse transcription-polymerase chain reaction (RT-PCR). Quantitative and morphological changes of GAP-43 and phospho-GAP-43 at P18 were assessed by western blot and immunohistochemical analyses.
Results: :
As well as GAP-43 mRNA, GAP-43 and phospho-GAP-43 protein levels increased in the retinas of OIR rats at P18 compared with the control. TA reduced the expression of GAP-43 mRNA and the protein levels of GAP-43 and phospho-GAP-43. GAP-43-immunoreactivity (IR) appeared strongly in the inner plexiform layer (IPL) and was greater in the OIR rat retinas than the control. Phospho-GAP-43-IR was positive in the inner retinal layers and showed an great increase in the ganglion cell layer (GCL), the IPL, and outer photoreceptor segments in the OIR rat retinas compared with the control.
Conclusions: :
These data suggest that the expression of GAP-43 and phopho-GAP-43 may involve in vasoproliferative retinopathy. Downregulation of GAP-43 and phospho-GAP-43 induced by TA may play a role in the course.
Keywords: retina • retinopathy of prematurity • retina: neurochemistry