Protective effects of triamcinolone acetonide upon the upregulation and phosphorylation of GAP 43 in an animal model of retinopathy of prematurity

Acta Ophthalmol. 2010: 88: e217–e221

Abstract.

Purpose: The aim of the current study was to investigate the effects of triamcinolone acetonide (TA) upon the expression and phosphorylation of growth‐associated protein 43 (GAP 43) in the retinas of oxygen‐induced retinopathy (OIR) rats. Methods: Oxygen‐induced retinopathy was induced by exposing Sprague‐Dawley rats to hyperoxia (80% oxygen) from postnatal (P) days 2–14 and then returning the rats to normoxic conditions. Triamcinolone acetonide or a conditioned saline (control) was injected intravitreally into the right or left eye, respectively, of OIR rats at P15. We then assessed the molecular and histological changes in the expression of GAP 43 and phospho‐GAP 43 in OIR and control rat retinas, and also after treatment with TA by RT‐PCR, Western blotting and immunohistochemistry. Results: Growth‐associated protein 43 mRNA levels were found to be increased by 1.6‐fold (p = 0.001, n = 5) in the retinas of P18 OIR rats compared with the control rats. The protein levels of GAP 43 and phospho‐GAP43 were found to be elevated in the retina of P18 OIR rats (2.40‐ and 2.39‐fold greater than each control, p<0.001, n = 5, respectively). Immunoreactivities of GAP 43 and phospho‐GAP 43 were stronger in the inner plexiform layer in OIR rat retinas compared with the control. However, treatment with TA attenuated GAP 43 and phospho‐GAP 43 upregulation in the OIR retinas. Conclusion: Our results indicate that GAP 43 and phospho‐GAP 43 participate in retinal (potentially pathologic) changes following oxygen‐induced damage. Triamcinolone acetonide protects the retinal damage in relatively hypoxic retinas of OIR rats. Therefore, TA treatment does not induce the expression and phosphorylation of GAP 43 in OIR rat retinas.