scholarly journals AAV Mediated GDNF Secretion From Retinal Glia Slows Down Retinal Degeneration in a Rat Model of Retinitis Pigmentosa

2011 ◽  
Vol 19 (9) ◽  
pp. 1602-1608 ◽  
Author(s):  
Deniz Dalkara ◽  
Kathleen D Kolstad ◽  
Karen I Guerin ◽  
Natalie V Hoffmann ◽  
Meike Visel ◽  
...  
Keyword(s):  
Retinitis Pigmentosa ◽  
Retinal Degeneration ◽  
Rat Model

scholarly journals Proinsulin Slows Retinal Degeneration and Vision Loss in the P23H Rat Model of Retinitis Pigmentosa

2012 ◽  
Vol 23 (12) ◽  
pp. 1290-1300 ◽  
Author(s):  
Laura Fernández-Sánchez ◽  
Pedro Lax ◽  
Carolina Isiegas ◽  
Eduard Ayuso ◽  
José M. Ruiz ◽  
...  
Keyword(s):  
Retinitis Pigmentosa ◽  
Retinal Degeneration ◽  
Rat Model ◽  
Vision Loss

scholarly journals A rat model for retinitis pigmentosa with rapid retinal degeneration enables drug evaluation in vivo

2021 ◽  
Vol 23 (1) ◽  
Author(s):  
Chisato Inoue ◽  
Tamaki Takeuchi ◽  
Akira Shiota ◽  
Mineo Kondo ◽  
Yuji Nshizawa
Keyword(s):  
Retinitis Pigmentosa ◽  
Retinal Degeneration ◽  
Rat Model ◽  
Photoreceptor Cell ◽  
Photoreceptor Cells ◽  
Therapeutic Agents ◽  
Transgenic Rat ◽  
Cell Degeneration ◽  
Rat Strain

Abstract Background Although retinitis pigmentosa (RP) is most frequently studied in mouse models, rats, rabbits, and pigs are also used as animal models of RP. However, no studies have reported postnatal photoreceptor cell loss before complete development in these models. Here, we generated a transgenic rat strain, named the P347L rat, in which proline at position 347 in the rhodopsin protein was replaced with leucine. Results A pathological analysis of photoreceptor cells in the P347L rat model was performed, and drugs with potential use as therapeutic agents against RP were investigated. The data clearly showed rapid degeneration and elimination of the outer nuclear layer even before the photoreceptor cells were fully established in P347L rats. To test the usefulness of the P347L rat in the search for new therapeutic agents against RP, the effects of rapamycin on RP were investigated in this rat strain. The findings suggest that rapamycin promotes autophagy and autophagosomal uptake of the rhodopsin that has accumulated abnormally in the cytoplasm, thereby alleviating stress and delaying photoreceptor cell death. Conclusions In this RP model, the time to onset of retinal degeneration was less than that of previously reported RP models with other rhodopsin mutations, enabling quicker in vivo evaluation of drug efficacy. Administration of rapamycin delayed the photoreceptor cell degeneration by approximately 1 day.

scholarly journals The Effect of Cyanine Dye NK-4 on Photoreceptor Degeneration in a Rat Model of Early-Stage Retinitis Pigmentosa

2021 ◽  
Vol 14 (7) ◽  
pp. 694
Author(s):  
Shihui Liu ◽  
Toshihiko Matsuo ◽  
Mary Miyaji ◽  
Osamu Hosoya
Keyword(s):  
Retinitis Pigmentosa ◽  
Rat Model ◽  
Metal Ion ◽  
Toxic Substance ◽  
Cyanine Dye ◽  
Pathway Enrichment Analysis ◽  
Rna Seq ◽  
Pathway Enrichment ◽  
Metal Ion Homeostasis ◽  
Rcs Rats

The present study aimed to evaluate the effects of NK-4 on the apoptosis of photoreceptors in a rat model of retinitis pigmentosa and explore the mechanism underlying anti-apoptosis activity. The Royal College of Surgeons (RCS) rats received an intravitreous injection of NK-4 solution in the left eye and vehicle control in the right eye. Apoptosis was detected by TUNEL method in frozen sections of the eyes. The retinal tissues of the rats were dissected for RNA-seq analysis. Functional and pathway enrichment analyses of differentially expressed genes (DEGs) were performed by using Metascape and DAVID software. The expression levels of DEGs were confirmed by real-time quantitative PCR (RT-qPCR). The number of apoptotic cells decreased in the outer nuclear layer (ONL) and the thickness of the ONL was significantly thicker in the retina of NK-4-injected eyes, compared with control eyes. Five DEGs were identified by RNA-seq analysis, and Hmox1, Mt1, Atf5, Slc7a11, and Bdh2 were confirmed to be up-regulated by RT-qPCR. Functional and pathway enrichment analysis of the up-regulated genes showed that anti-apoptosis effects of NK-4 in the retina of RCS rats may be related to the pathways of metal ion homeostasis, negative regulation of neuron death, response to toxic substance, and pigment metabolic process. We found a potential mechanism of NK-4, providing a new viewpoint for the development of more therapeutic uses of NK-4 in the future.

Retinal blood vessels are damaged in a rat model of NMDA-induced retinal degeneration

2010 ◽  
Vol 485 (1) ◽  
pp. 55-59 ◽  
Author(s):  
Kaori Ueda ◽  
Tsutomu Nakahara ◽  
Maya Hoshino ◽  
Asami Mori ◽  
Kenji Sakamoto ◽  
...  
Keyword(s):  
Blood Vessels ◽  
Retinal Degeneration ◽  
Rat Model ◽  
Retinal Blood Vessels

Short-term high-fat feeding exacerbates degeneration in retinitis pigmentosa by promoting retinal oxidative stress and inflammation

2021 ◽  
Vol 118 (43) ◽  
pp. e2100566118
Author(s):  
Oksana Kutsyr ◽  
Agustina Noailles ◽  
Natalia Martínez-Gil ◽  
Lucía Maestre-Carballa ◽  
Manuel Martinez-Garcia ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Retinitis Pigmentosa ◽  
Retinal Degeneration ◽  
Gut Microbiome ◽  
Cell Activation ◽  
High Fat ◽  
Short Term ◽  
Oxidative Markers ◽  
Degenerative Disorders ◽  
Inflammatory State

A high-fat diet (HFD) can induce hyperglycemia and metabolic syndromes that, in turn, can trigger visual impairment. To evaluate the acute effects of HFD feeding on retinal degeneration, we assessed retinal function and morphology, inflammatory state, oxidative stress, and gut microbiome in dystrophic retinal degeneration 10 (rd10) mice, a model of retinitis pigmentosa, fed an HFD for 2 to 3 wk. Short-term HFD feeding impaired retinal responsiveness and visual acuity and enhanced photoreceptor degeneration, microglial cell activation, and Müller cell gliosis. HFD consumption also triggered the expression of inflammatory and oxidative markers in rd10 retinas. Finally, an HFD caused gut microbiome dysbiosis, increasing the abundance of potentially proinflammatory bacteria. Thus, HFD feeding drives the pathological processes of retinal degeneration by promoting oxidative stress and activating inflammatory-related pathways. Our findings suggest that consumption of an HFD could accelerate the progression of the disease in patients with retinal degenerative disorders.

scholarly journals Microglia dynamics in retinitis pigmentosa model: formation of fundus whitening and autofluorescence as an indicator of activity of retinal degeneration

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Kenichi Makabe ◽  
Sunao Sugita ◽  
Michiko Mandai ◽  
Yoko Futatsugi ◽  
Masayo Takahashi
Keyword(s):  
Retinitis Pigmentosa ◽  
Retinal Degeneration ◽  
Outer Nuclear Layer ◽  
Fundus Autofluorescence ◽  
Fundus Photography ◽  
Photoreceptor Outer Segments ◽  
Diagnostic Interpretation ◽  
Model Formation ◽  
Thinning Rate

Abstract In patients with retinitis pigmentosa (RP), color fundus photography and fundus autofluorescence (FAF) have been used to estimate the disease progression. To understand the origin and the diagnostic interpretation of the fundus color and FAF, we performed in vivo imaging of fundus color and FAF together with histological analyses of the retinal degeneration process using the RP model mice, rd10. FAF partly represented the accumulation of microglia in the photoreceptor outer segments. Fundus whitening suggested the presence of apoptotic cells, which spatiotemporally preceded increase in FAF. We observed two patterns of FAF localization, arcuate and diffuse, each indicating different pattern of apoptosis, wavy and diffuse, respectively. Diffuse pattern of apoptosis was suppressed in dark-raised rd10 mice, in which outer nuclear layer (ONL) loss was significantly suppressed. The occupancy of FAF correlated with the thinning rate of the ONL. Fractalkine, a microglia chemotactic factor, was detected in apoptotic photoreceptors, suggesting chemokine-induced recruitment of microglia into the ONL, which paralleled with accelerated ONL loss and increased FAF occupancy. Thus, we propose that the degree of photoreceptor apoptosis and the rate of ONL thinning in RP patients might be read from the fundus color and the FAF.

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