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N. Wang, Y. Wei, J. Li; Enhanced Protein Expression of ProNGF Could Not Active TrkA Following Elevated Intraocular Pressure-Induced Rat Retinal Ischemia. Invest. Ophthalmol. Vis. Sci. 2008;49(13):768. doi: https://doi.org/.
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© ARVO (1962-2015); The Authors (2016-present)
To investigate the protein expression change of proNGF in rat retina after elevated intraocular pressure (IOP)-induced retinal ischemia and its relationship with expression of NGF and TrkA.
The IOP was increased to 110mmHg for 60 min by anterior chamber cannulation in the right eye and sham-procedure was done in the left eye. Time-course examination was performed at 1h, 1, 3, 5, and 7 days after elevated IOP-induced retinal ischemia. Expression of proNGF, NGF and TrkA was evaluated by immunoblot analysis, proNGF and neurofilaments were double labeled by immunohistochemistry at frozen retina slice to ascertain the cell types of proNGF positive cells. Statistical analysis was conducted by one-way analysis of variance, followed by all pairwise multiple comparison procedures using Bonferroni test. Significance was regarded as at least p<0.05.
Western blot analysis showed the expression of proNGF at the band of 28KD, 32KD, 46KD, 53KD and 60KD (glycosylated pieces). The protein expressions of 46KD and 53KD increased significantly (p<0.05) at day 3, 5 and 7 after retinal ischemia. proNGF was primarily present in nerve fiber layer (NFL) and large ganglion cells bodies. 14KD NGF and TrkA increased weakly after retinal ischemia.
The glycosylated 46KD and 53-KD protein of ProNGF might have key role in the apoptosis pathway of retinal cells after IOP induced retina ischemia. Increased proNGF might elicit death signal which may be transduced by the p75NTR-sortilin receptor complex or by p75NTR itself. This needs further investigation.
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