Purpose: To assess the vulnerability of retinal photoreceptors in the BALB/cJ, C57BL/6J, and C57BL/6-c2J (c2J) mouse strains to hypoxic and hyperoxic stress.
Methods: Mice were raised in dim cyclic light. Pups aged postnatal day 7 (P7) were exposed to hypoxia (11-12% oxygen) for periods up to 23 days. Adult mice were exposed to either hypoxia (12% oxygen) or to hyperoxia (75% oxygen) for up to 2 weeks. Using the TUNEL (terminal dUTP-mediated nick end labeling) technique retinas were examined for cell death.
Results: In juvenile mice, hypoxia induced a robust increase in photoreceptor death in the C57BL/6J strain and a weaker increase in the C57BL/6-c2J strains. In the adult, hypoxia was associated with a small reduction in photoreceptor death in the C57BL/6-c2J strains. Hyperoxia caused substantial photoreceptor death in both the C57BL/6-c2J and C57BL/6J strains. The BALB/cJ strain was more resistant to oxygen stress than the C57BL strains.
Conclusions: The difference in oxygen vulnerability between C57BL/6J and BALB/c strains may provide a useful starting point for the analysis of genetic regulation of this vulnerability. The resistance of the C57BL/6-c2J substrains to hypoxia may reflect their degenerative status.
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http://dx.doi.org/10.1080/02713680490522416 | DOI Listing |
Cells
January 2025
Department of Pharmacology, School of Medicine, Case Western Reserve University, 10900 Euclid Ave., Cleveland, OH 44106, USA.
Retinitis pigmentosa (RP) is a hereditary disease characterized by progressive vision loss ultimately leading to blindness. This condition is initiated by mutations in genes expressed in retinal cells, resulting in the degeneration of rod photoreceptors, which is subsequently followed by the loss of cone photoreceptors. Mutations in various genes expressed in the retina are associated with RP.
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January 2025
Department of Ophthalmology, Ruijin Hospital, Affiliated Shanghai Jiaotong University School of Medicine, 197 Ruijin Er Road, Shanghai, 200025, China.
VEGF is not only the most potent angiogenic factor, but also an important neurotrophic factor. In this study, vitreous expression of six neurotrophic factors were examined in proliferative diabetic retinopathy (PDR) patients with prior anti-VEGF therapy (n = 48) or without anti-VEGF treatment (n = 41) via ELISA. Potential source, variation and impact of these factors were further investigated in a mouse model of oxygen-induced retinopathy (OIR), as well as primary Müller cells and 661W photoreceptor cell line under hypoxic condition.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN 38163, USA.
Retinal degenerative diseases lead to irreversible vision loss due to photoreceptor cell death, driven by complex genetic and environmental factors. Ceramide, a sphingolipid metabolite, emerges as a critical mediator in the apoptotic cascade associated with retinal degeneration. Our previous work demonstrated L-Cycloserine's ability to protect photoreceptor-derived cells from oxidative stress by inhibiting the de novo ceramide pathway and thus prompting further investigation on its effect in the in vivo retina.
View Article and Find Full Text PDFMedicina (Kaunas)
December 2024
Ophthalmology Laboratory, Neuroscience Institute, Lithuanian University of Health Sciences, Medical Academy, Eiveniu 2, LT-50161 Kaunas, Lithuania.
: Age-related macular degeneration (AMD) is the leading cause of blindness, affecting millions worldwide. Its pathogenesis involves the death of the retinal pigment epithelium (RPE), followed by photoreceptor degeneration. Although AMD is multifactorial, various genetic markers are strongly associated with the disease and may serve as biomarkers for evaluating treatment efficacy.
View Article and Find Full Text PDFNeurobiol Dis
December 2024
Department of Physiology & Neuroscience, Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA. Electronic address:
Huntington's disease (HD) is caused by the expansion of a CAG repeat, encoding a string of glutamines (polyQ) in the first exon of the huntingtin gene (HTTex1). This mutant huntingtin protein (mHTT) with extended polyQ forms aggregates in cortical and striatal neurons, causing cell damage and death. The retina is part of the central nervous system (CNS), and visual deficits and structural abnormalities in the retina of HD patients have been observed.
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