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[Effect of VEGF-B on neuroprotection in mouse retinal ganglion cells].

S Zhang, Yi Qu

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Abstract

OBJECTIVE: To investigate the expression of vascular endothelial growth factor-B (VEGF-B) in retina and its effect on neuroprotection in mouse retinal ganglion cells (RGCs). METHODS: It was a experimental study. 35 of C57BL/6 mice (adult male) were used. Optic nerve crush injury was made in 28 mice, 7 as control. Expression of VEGF-B in retina was detected by hybridization in situ in each group of 2 at 6 hours, 1 day, 1 and 2 weeks after optic nerve crush. A quantitative analysis of VEGF-B mRNA was determined by real time reverse transcription polymerase chain reaction (RT-PCR) in each group of 5 at 6 hours, 1 day, 1 and 2 weeks after optic nerve crush. Additional 36 mice were divided into 4 groups: control (8), optic nerve crush (9), optic nerve crash plus PBS intravitreal injection (7), and optic nerve crash plus VEGF-B (450 mg/L) intravitreal injection (12). RGCs were counted by retrograde tracing of Fluorogold to evaluate the effect of VEGF-B on neuroprotection by microscope. RESULTS: Compared with control group, the expression of VEGF-B was significantly increased in the retina of mice and peaked at one week after the optic nerve crush. The number of RGCs was 1.7 fold higher in optic nerve crush alone and 1.9 fold higher in optic nerve crush combined with intravitreal injection of VEGF-B, which reached statistically significance (t = 0.001, P < 0.01 and t = 0.001, P < 0.01, respectively). CONCLUSIONS: Our results indicate that VEGF-B is involved in the retinal recovery processes and plays a potent role of neuroprotection in RGCs after the optic nerve crush.

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What this paper is about

OBJECTIVE: To investigate the expression of vascular endothelial growth factor-B (VEGF-B) in retina and its effect on neuroprotection in mouse retinal ganglion cells (RGCs). METHODS: It was a experimental study. 35 of C57BL/6 mice (adult male) were used. Optic nerve crush injury was made in 28 mice, 7 as control. Expression of VEGF-B in retina was detected by hybridization in situ in each group of 2 at 6 hours, 1 day, 1 and 2 weeks after optic nerve crush. A quantitative analysis of VEGF-B mRNA was determined by real time reverse transcription polymerase chain reaction (RT-PCR) in each group of 5 at 6 hours, 1 day, 1 and 2 weeks after optic nerve crush. Additional 36 mice were divided into 4 groups: control (8), optic nerve crush (9), optic nerve crash plus PBS intravitreal injection (7), and optic nerve crash plus VEGF-B (450 mg/L) intravitreal injection (12). RGCs were counted by retrograde tracing of Fluorogold to evaluate the effect of VEGF-B on neuroprotection by microscope. RESULTS: Compared with control group, the expression of VEGF-B was significantly increased in the retina of mice and peaked at one week after the optic nerve crush. The number of RGCs was 1.7 fold higher in optic nerve crush alone and 1.9 fold higher in optic nerve crush combined with intravitreal injection of VEGF-B, which reached statistically significance (t = 0.001, P < 0.01 and t = 0.001, P < 0.01, respectively). CONCLUSIONS: Our results indicate that VEGF-B is involved in the retinal recovery processes and plays a potent role of neuroprotection in RGCs after the optic nerve crush.

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Available abstract

OBJECTIVE: To investigate the expression of vascular endothelial growth factor-B (VEGF-B) in retina and its effect on neuroprotection in mouse retinal ganglion cells (RGCs). METHODS: It was a experimental study. 35 of C57BL/6 mice (adult male) were used. Optic nerve crush injury was made in 28 mice, 7 as control. Expression of VEGF-B in retina was detected by hybridization in situ in each group of 2 at 6 hours, 1 day, 1 and 2 weeks after optic nerve crush. A quantitative analysis of VEGF-B mRNA was determined by real time reverse transcription polymerase chain reaction (RT-PCR) in each group of 5 at 6 hours, 1 day, 1 and 2 weeks after optic nerve crush. Additional 36 mice were divided into 4 groups: control (8), optic nerve crush (9), optic nerve crash plus PBS intravitreal injection (7), and optic nerve crash plus VEGF-B (450 mg/L) intravitreal injection (12). RGCs were counted by retrograde tracing of Fluorogold to evaluate the effect of VEGF-B on neuroprotection by microscope. RESULTS: Compared with control group, the expression of VEGF-B was significantly increased in the retina of mice and peaked at one week after the optic nerve crush. The number of RGCs was 1.7 fold higher in optic nerve crush alone and 1.9 fold higher in optic nerve crush combined with intravitreal injection of VEGF-B, which reached statistically significance (t = 0.001, P < 0.01 and t = 0.001, P < 0.01, respectively). CONCLUSIONS: Our results indicate that VEGF-B is involved in the retinal recovery processes and plays a potent role of neuroprotection in RGCs after the optic nerve crush.

Key concepts: Optic nerve, Crush injury, Neuroprotection, Retina, Ganglion cell layer, Retinal ganglion cell, Retinal, Ophthalmology

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