Abstract
Purpose: :
Glaucoma is a group of diseases in which optic nerve is damaged and lead to bilateral blindness. It is known that retinal ganglion cells in primary open-angle glaucoma (POAG) death by apoptosis. Poly (ADP-ribose) polymerase-1 (PARP-1) has a role in DNA damage repair, but PARP-1 could be cleaved by caspase-3 so that prevents the repair of DNA and facilitates the initiation of apoptosis. Other proteins protect cells from apoptosis. Brain-derived neurotrophic factor (BDNF) is a protein that promotes the survival of ganglion cells by inhibiting apoptosis and increasing axonal elongation. Vascular endothelial growth factor (VEGF) also inhibits apoptosis by means the induction of anti-apoptotic proteins (e.g. Bcl-2). The aim of this study is to evaluate if these pro-apoptotic and anti-apoptotic proteins could be useful as a markers of cell death in POAG.
Methods: :
A case-control study was performed in 41 patients with POAG and 50 patients with non-pathological cataracts. A sample of aqueous humor from each subject was obtained at the beginning of the surgical procedures. BDNF and VEGF levels were determined using a commercial EIA kit from R&D Systems. The expression of caspase-3 and PARP-1 was carried out by Western blot. Data were processed for Statistical Analysis using the SPSS v.15.0 (SPSS Inc., Chicago, IL, USA)
Results: :
BDNF and VEGF levels were statistically significant lower in POAG group than in cataracts group ([BDNF: 98,1 ± 8,2 pg/mL in POAG and 111,3 ± 11,6 pg/mL in cataracts; p=0.0008]; [VEGF: 65,2 ± 5,5 pg/mL in POAG and 76,9 ± 9,8 pg/mL in cataracts; p=0.0003]). Expression of caspase-3 and PARP-1 were statistically higher in POAG group than in cataracts group ([PARP-1 85kDa: 58,7 ± 7,5 DU in POAG and 19,2 ± 3,2 DU in cataracts; p=0.001]; [PARP-1 24kDa: 44,2 ± 6,5 DU in POAG and 6,6 ± 3,1 DU in cataracts; p=0.013]; [Caspase-3: 76,1 ± 7,4 DU in POAG and 68,3 ± 8,6 DU in cataracts; p=0.018])
Conclusions: :
These proteins may be used as a marker of neuronal damage and could help us to prevent the glaucomatous blindness.
Keywords: apoptosis/cell death • neuroprotection • visual impairment: neuro-ophthalmological disease