Purpose : Retina is a highly vascularized tissue and a proper balance between hypoxia and hyperoxia is required to maintain an healthy status. It is known that Light Damage (LD) induces photoreceptors death and vision loss but little is known about the consequences on vascularization. The aim of our research was to characterize the vascularization changes that occur in a retina affected by LD. Methods : Sprague Dawley albino rats were exposed to 1000 Lux light for 24 hours: one group recovered for 7 days (LD+7rec) and the second one for 60 days (LD+60rec). To identify retinal vessels, Isolectin immunostaining was performed on retinal whole mounts of LD and control animals. The images of each retinal layer were aquired in the central, nasal and temporal regions of the dorsal retina by a confocal microscope and then analyzed by “Angio Tool” software. The levels of VEGF were quantified by Western blot (WB). Results : LD+7rec retinas showed a significantly increased vascularization in the inner nuclear layer (INL), inner plexiform layer (IPL) and ganglion cell layer (GCL) of the dorsal retina, considering vessels percentage area, vessels length and blebs of neovascularization. We found that blebs were increased in all the inner layers at the central (GCL:p<0,001; IPL:p=0,045; INL:p=0,018), nasal (GCL:p<0,001; IPL:p=0,017; INL:p=0.049) and temporal (GCL:p=0,012; IPL:p=0,018; INL:p=0,001) regions of the dorsal retina. The INL was characterized by a higher density of vessels since the percentage vessels area was increased (centre:p=0,034; nasal:p=0,048; temporal:p=0,041). No new vessels, instead, were observed in the outer nuclear layer. WB results confirmed histological analysis, since VEGF was increased in LD animals compared to the controls (p=0,01). LD+60rec retinas showed a decrease in the vessels percentage area (p=0.009) as well as in the number of blebs in the INL (p=0,011) compared to LD+7rec. Anyway, vessels morphology was clearly disorganized. Conclusions : Our study demonstrates that light damage induces retinal neovascularization after 7 days of recovery and this is linked to the higher expression of VEGF. A longer recovery (60 days), instead, leads to the disruption of the vessels network. We can therefore assume that this model can be used to test new therapies against retinal pathologies where vascularization is compromised.
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