scholarly journals Attenuation of Vision Loss and Delay in Apoptosis of Photoreceptors Induced by Proinsulin in a Mouse Model of Retinitis Pigmentosa

2008 ◽  
Vol 49 (9) ◽  
pp. 4188 ◽  
Author(s):  
Silvia Corrochano ◽  
Rima Barhoum ◽  
Patricia Boya ◽  
Ana I. Arroba ◽  
Natalia Rodri´guez-Muela ◽  
...  
Pharmaceutics ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 913
Author(s):  
Ander Anasagasti ◽  
Araceli Lara-López ◽  
Santiago Milla-Navarro ◽  
Leire Escudero-Arrarás ◽  
María Rodríguez-Hidalgo ◽  
...  

Inherited retinal dystrophies (IRDs) are a group of rare retinal conditions, including retinitis pigmentosa (RP), caused by monogenic mutations in 1 out of more than 250 genes. Despite recent advancements in gene therapy, there is still a lack of an effective treatment for this group of retinal conditions. MicroRNAs (miRNAs) are a class of highly conserved small non-coding RNAs that inhibit gene expression. Control of miRNAs-mediated protein expression has been described as a widely used mechanism for post-transcriptional regulation in many physiological and pathological processes in different organs, including the retina. Our main purpose was to test the hypothesis that modulation of a group of miRNAs can protect photoreceptor cells from death in the rd10 mouse model of retinitis pigmentosa. For this, we incorporated modulators of three miRNAs in adeno-associated viruses (AAVs), which were administered through sub-retinal injections. The results obtained indicate that inhibition of the miR-6937-5p slows down the visual deterioration of rd10 mice, reflected by an increased electroretinogram (ERG) wave response under scotopic conditions and significant preservation of the outer nuclear layer thickness. This work contributes to broadening our knowledge on the molecular mechanisms underlying retinitis pigmentosa and supports the development of novel therapeutic approaches for RP based on miRNA modulation.


2021 ◽  
Author(s):  
Johanna E Wagner ◽  
Lena Zobel ◽  
Maximilian Joachim Gerhardt ◽  
Catherine R O'Riordan ◽  
Amy Frederick ◽  
...  

Recent developments in understanding the pathophysiology of retinitis pigmentosa (RP) have shown that there have been new hopes in the treatment of this disease which can cause severe vision loss. Proven therapy for RP-associated photoreceptor loss and retinal pigment epithelial damage has not yet been reported. New or experimental approaches for the treatment of RP include platelet-rich plasma, gene therapy, transplantation of fetal retinal cells or stem cells, and electronic retinal prostheses.


2019 ◽  
Vol 20 (3) ◽  
pp. 714
Author(s):  
Mor Dahbash ◽  
Ruti Sella ◽  
Elinor Megiddo-Barnir ◽  
Yael Nisgav ◽  
Nataly Tarasenko ◽  
...  

: Choroidal neovascularization (CNV) is a complication of age-related macular degeneration and a major contributing factor to vision loss. In this paper, we show that in a mouse model of laser-induced CNV, systemic administration of Butyroyloxymethyl-diethyl phosphate (AN7), a histone deacetylase inhibitor (HDACi), significantly reduced CNV area and vascular leakage, as measured by choroidal flatmounts and fluorescein angiography. CNV area reduction by systemic AN7 treatment was similar to that achieved by intravitreal bevacizumab treatment. The expression of vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF-2), and the endothelial cells marker CD31, was lower in the AN7 treated group in comparison to the control group at the laser lesion site. In vitro, AN7 facilitated retinal pigmented epithelium (RPE) cells tight junctions’ integrity during hypoxia, by protecting the hexagonal pattern of ZO-1 protein in the cell borders, hence reducing RPE permeability. In conclusion, systemic AN7 should be further investigated as a possible effective treatment for CNV.


2019 ◽  
Vol 288 ◽  
pp. 337-346 ◽  
Author(s):  
Miguel Cabello ◽  
Marta Mozo ◽  
Berta De la Cerda ◽  
Carmen Aracil ◽  
Francisco J. Diaz-Corrales ◽  
...  

2015 ◽  
Vol 111 ◽  
pp. 197-207 ◽  
Author(s):  
Samantha I. Cunningham ◽  
James D. Weiland ◽  
Pinglei Bao ◽  
Gilberto Raul Lopez-Jaime ◽  
Bosco S. Tjan

2019 ◽  
Vol 63 (11) ◽  
Author(s):  
Tatsuma Kishimoto ◽  
Waka Ishida ◽  
Ken Fukuda ◽  
Isana Nakajima ◽  
Takashi Suzuki ◽  
...  

ABSTRACT Endophthalmitis due to infection with Enterococcus spp. progresses rapidly and often results in substantial and irreversible vision loss. Given that the frequency of this condition caused by vancomycin-resistant Enterococcus faecalis has been increasing, the development of novel therapeutics is urgently required. We have demonstrated the therapeutic potential of bacteriophage ΦEF24C-P2 in a mouse model of endophthalmitis caused by vancomycin-sensitive (EF24) or vancomycin-resistant (VRE2) strains of E. faecalis. Phage ΦEF24C-P2 induced rapid and pronounced bacterial lysis in turbidity reduction assays with EF24, VRE2, and clinical isolates derived from patients with E. faecalis-related postoperative endophthalmitis. Endophthalmitis was induced in mice by injection of EF24 or VRE2 (1 × 104 cells) into the vitreous. The number of viable bacteria in the eye increased to >1 × 107 CFU, and neutrophil infiltration into the eye was detected as an increase in myeloperoxidase activity at 24 h after infection. A clinical score based on loss of visibility of the fundus as well as the number of viable bacteria and the level of myeloperoxidase activity in the eye were all significantly decreased by intravitreous injection of ΦEF24C-P2 6 h after injection of EF24 or VRE2. Whereas histopathologic analysis revealed massive infiltration of inflammatory cells and retinal detachment in vehicle-treated eyes, the number of these cells was greatly reduced and retinal structural integrity was preserved in phage-treated eyes. Our results thus suggest that intravitreous phage therapy is a potential treatment for endophthalmitis caused by vancomycin-sensitive or -resistant strains of E. faecalis.


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