Microarray analysis of retinal gene expression in the DBA/2J model of glaucoma
Abstract
Purpose The DBA/2J mouse is a model for secondary angle-closure glaucoma, due to iris atrophy and pigment dispersion, which ultimately lead to increased intraocular pressure (IOP). The study was undertaken to correlate changes in retinal gene expression with IOP elevation by performing microarray analysis of retinal RNA from DBA/2J mice at 3 months before disease onset and at 8 months after IOP elevation. Methods IOP was monitored monthly in DBA/2J animals, and animals with normal (3 months) or elevated IOP (8 months) were identified. RNA was prepared from three individual retinas at each age, and the RNA was amplified and used to generate biotin-labeled probe for high-density mouse gene microarrays (U430.2; Affymetrix, Santa Clara, CA). A subset of genes was selected for confirmation by quantitative RT-PCR, by using independent retina samples from DBA/2J animals at 3, 5, and 8 months of age and compared to retinas from C57BL/6J control animals at 3 and 8 months. Results There were changes in expression of 68 genes, with 32 genes increasing and 36 genes decreasing at 8 months versus 3 months. Upregulated genes were associated with immune response, glial activation, signaling, and gene expression, whereas downregulated genes included multiple crystallin genes. Significant changes in nine upregulated genes and two downregulated genes were confirmed by quantitative RT-PCR, with some showing changes in expression by 5 months. Conclusions DBA/2J retina shows evidence of glial acti…
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In a mouse model of glaucoma, C1q and C3 are highly upregulated and deposited on retinal synapses, and C1q deficiency or microglial inactivation with minocycline provides significant neuroprotection.
“Indeed, in a mouse model of glaucoma, a neurodegenerative disease associated with RGC loss and gliosis, C1q and C3 are highly upregulated and deposited on retinal synapses and C1q deficiency or microglial ‘inactivation’ with minocycline provide significant neuroprotection (Howell et al., 2011; Steele et al., 2006; Stevens et al., 2007).”
From Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner (2012) · cites this paper as Steele et al., 2006
Cites
Zareparsi, S., Branham, K. E. H., Li, M., Shah, S., Klein, R. J., Ott, J., Hoh, J., Abecasis, G. R., & Swaroop, A. (2005) · The American Journal of Human Genetics · doi:10.1086/431426 · Cited by 371 · see citing works
Flagged first, then by citations
Cited by
Sorted by citations
Microglia Sculpt Postnatal Neural Circuits in an Activity and Complement-Dependent Manner
Schafer, D. P., Lehrman, E. K., Kautzman, A. G., Koyama, R., Mardinly, A. R., Yamasaki, R., Ransohoff, R. M., Greenberg, M. E., Barres, B. A., & Stevens, B. (2012) · Neuron · doi:10.1016/j.neuron.2012.03.026 · Cited by 4,089 · see citing works
The Classical Complement Cascade Mediates CNS Synapse Elimination
Stevens, B., Allen, N. J., Vazquez, L. E., Howell, G. R., Christopherson, K. S., Nouri, N., Micheva, K. D., Mehalow, A. K., Huberman, A. D., Stafford, B., et al. (2007) · Cell · doi:10.1016/j.cell.2007.10.036 · Cited by 3,313 · see citing works
The Complement System: An Unexpected Role in Synaptic Pruning During Development and Disease
Stephan, A. H., Barres, B. A., & Stevens, B. (2012) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-061010-113810 · Cited by 1,113 · see citing works
Role of Inflammation in Diabetic Retinopathy
Rübsam, A., Parikh, S., & Fort, P. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19040942 · Cited by 750 · see citing works
Microglia activation in retinal degeneration
Langmann, T. (2007) · Journal of Leukocyte Biology · doi:10.1189/jlb.0207114 · Cited by 496 · see citing works
Howell, G. R., Macalinao, D. G., Sousa, G. L., Walden, M., Soto, I., Kneeland, S. C., Barbay, J. M., King, B. L., Marchant, J. K., Hibbs, M., et al. (2011) · Journal of Clinical Investigation · doi:10.1172/jci44646 · Cited by 473 · see citing works
The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma.
Ramirez, A. I., de Hoz, R., Salobrar-Garcia, E., Salazar, J. J., Rojas, B., Ajoy, D., López-Cuenca, I., Rojas, P., Triviño, A., & Ramírez, J. M. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00214 · Cited by 466 · see citing works
Gallego, B. I., Salazar, J. J., de Hoz, R., Rojas, B., Ramírez, A. I., Salinas-Navarro, M., Ortín-Martínez, A., Valiente-Soriano, F. J., Avilés-Trigueros, M., Villegas-Perez, M. P., et al. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-92 · Cited by 224 · see citing works
The microglia in healthy and diseased retina
Li, L., Eter, N., & Heiduschka, P. (2015) · Experimental Eye Research · doi:10.1016/j.exer.2015.04.020 · Cited by 112 · see citing works
The Role of the Classical Complement Cascade in Synapse Loss During Development and Glaucoma
Rosen, A. M., & Stevens, B. (2010) · Advances in Experimental Medicine and Biology · doi:10.1007/978-1-4419-5635-4_6 · Cited by 60 · see citing works
MicroRNA Expression in the Glaucomatous Retina
Jayaram, H., Cepurna, W. O., Johnson, E. C., & Morrison, J. C. (2015) · Investigative Opthalmology & Visual Science · doi:10.1167/iovs.15-18088 · Cited by 60 · see citing works
Lambert, W. S., Pasini, S., Collyer, J. W., Formichella, C. R., Ghose, P., Carlson, B. J., & Calkins, D. J. (2020) · Scientific Reports · doi:10.1038/s41598-020-65374-6 · Cited by 21 · see citing works
Self-citation
- Authors
- Steele, M. R., Inman, D. M., Calkins, D. J., Horner, P. J., & Vetter, M. L.
- Affiliations
- University of Utah (US)
- University of Washington (US)
- Vanderbilt University (US)
- Venue
- Investigative Opthalmology & Visual Science
- Published
- 2006-03-01
- Volume
- 47
- Issue
- 3
- Pages
- 977
- ISSN
- 0146-0404 (ISSN-L)
- 1552-5783
- OpenAlex
- W1964675499
- Cited by
- 196
- References
- 1
- Citations by year
- 2025: 1 · 2024: 3 · 2023: 5 · 2022: 6 · 2021: 10 · 2020: 5 · 2019: 7 · 2018: 10 · 2017: 9 · 2016: 5 · 2015: 10 · 2014: 12 · 2013: 12 · 2012: 16
- FWCI
- 13.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Investigative Ophthalmology & Visual Science (publishedVersion, public-domain)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Ophthalmology › Glaucoma and retinal disorders
- Health Sciences › Medicine › Ophthalmology › Retinal Diseases and Treatments
- Health Sciences › Medicine › Ophthalmology › Drug-Induced Ocular Toxicity
- Keywords
- DBA/2J mice, secondary angle-closure glaucoma, retinal gene expression, intraocular pressure elevation, iris atrophy, pigment dispersion, glial activation, immune response, crystallin genes, retinal transcriptome
- MeSH terms
- Animals, Disease Models, Animal, Female, Intraocular Pressure, Mice, Inbred C57BL, Mice, Inbred DBA, Retina, RNA, Messenger, Tonometry, Ocular, Glaucoma, Angle-Closure, Up-Regulation, Gene Expression, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, Gene Expression Profiling, Mice
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
