Time course analysis of gene expression during light‐induced photoreceptor cell death and regeneration in albino zebrafish
Abstract
Constant intense light causes apoptosis of rod and cone photoreceptors in adult albino zebrafish. The photoreceptors subsequently regenerate from proliferating inner nuclear layer (INL) progenitor cells that migrate to the outer nuclear layer (ONL) and differentiate into rods and cones. To identify gene expression changes during this photoreceptor regeneration response, a microarray analysis was performed at five time points during the light treatment. The time course included an early time point during photoreceptor death (16 h), later time points during progenitor cell proliferation and migration (31, 51, and 68 h) and a 96 h time point, which likely corresponds to the initial photoreceptor differentiation. Mean expression values for each gene were calculated at each time point relative to the control (0 h light exposure) and statistical analysis by one‐way ANOVA identified 4567 genes exhibiting significant changes in gene expression along the time course. The genes within this data set were clustered based on their temporal expression patterns and proposed functions. Quantitative real‐time PCR validated the microarray expression profiles for selected genes, including stat3 whose expression increased markedly during the light exposure. Based on immunoblots, both total and activated Stat3 protein expression also increased during the light treatment. Immunolocalization of Stat3 on retinal tissue sections demonstrated increased expression in photoreceptors and Müller glia by 16 h of light exposure. Some of the Stat3‐positive Müller cells expressed PCNA at 31 h, suggesting that Stat3 may play a role in signaling a subset of Müller cells to proliferate during the regeneration response. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007.
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Zebrafish Müller glia respond to retinal injury by producing multipotent progenitors that repair the retina.
“Müller glia (MG) in the zebrafish retina respond to retinal injury by generating multipotent progenitors for retinal repair.”
From Retinal injury, growth factors, and cytokines converge on β-catenin and pStat3 signaling to stimulate retina regeneration (2014) · cites this paper as Kassen et al., 2007
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Self-citationFgf signaling is required for photoreceptor maintenance in the adult zebrafish retina
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- Authors
- Kassen, S. C., Ramanan, V., Montgomery, J. E., T. Burket, C., Liu, C., Vihtelic, T. S., & Hyde, D. R.
- Affiliations
- University of Notre Dame (US)
- Thomas Jefferson University (US)
- Corresponding author
- Hyde, David R.
- Venue
- Developmental Neurobiology
- Publisher
- Wiley
- Published
- 2007-03-06
- Volume
- 67
- Issue
- 8
- Pages
- 1009-1031
- ISSN
- 1932-8451 (ISSN-L)
- 1932-846X
- OpenAlex
- W1976517931
- Cited by
- 203
- References
- 66
- Citations by year
- 2026: 2 · 2025: 7 · 2024: 6 · 2023: 19 · 2022: 7 · 2021: 14 · 2020: 7 · 2019: 10 · 2018: 7 · 2017: 13 · 2016: 9 · 2015: 14 · 2014: 10 · 2013: 14 · 2012: 15
- FWCI
- 4.77
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Developmental Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Eye Institute (R21EY017134)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Retinal Development and Disorders
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Keywords
- photoreceptor cell death, photoreceptor regeneration, rod photoreceptors, cone photoreceptors, Müller cells, STAT3, temporal gene expression, light-induced retinal damage, PCNA
- MeSH terms
- Albinism, Animals, Cell Division, Fish Diseases, Gene Expression Regulation, Kinetics, Light, Photoreceptor Cells, Retina, Retinal Degeneration, Zebrafish, Cell Death, Apoptosis, Genes, Reporter, Retinal Rod Photoreceptor Cells, Retinal Cone Photoreceptor Cells, Oligonucleotide Array Sequence Analysis, Animals, Genetically Modified, Green Fluorescent Proteins
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