ArticleThe American journal of pathology2011
A role for vascular deficiency in retinal pathology in a mouse model of ataxia-telangiectasia.
Article in The American journal of pathology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Recent Advances in Therapy for the Neurodegenerative Disorder Ataxia-Telangiectasia.International journal of molecular sciences · 2026Review
- Computational modeling of ATM signaling: a predictive framework for drug repurposing in ataxia-telangiectasia.NPJ systems biology and applications · 2025Article
- Ataxia-telangiectasia mutated plays an important role in cerebellar integrity and functionality.Neural regeneration research · 2023Review
- Transcriptomic Analysis of circRNAs in the Peripheral Blood of Nonarteritic Anterior Ischemic Optic Neuropathy.BioMed research international · 2020Article
- Astrocytes restore connectivity and synchronization in dysfunctional cerebellar networks.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Ataxia telangiectasia: a review.Orphanet journal of rare diseases · 2016Review
- Connecting Malfunctioning Glial Cells and Brain Degenerative Disorders.Genomics, proteomics & bioinformatics · 2016Review
- Cerebral abnormalities in adults with ataxia-telangiectasia.AJNR. American journal of neuroradiology · 2014Article
- The ATM protein kinase: regulating the cellular response to genotoxic stress, and more.Nature reviews. Molecular cell biology · 2013Review
- Pathological neoangiogenesis depends on oxidative stress regulation by ATM.Nature medicine · 2012Article
- The role of the neuro-astro-vascular unit in the etiology of ataxia telangiectasia.Frontiers in pharmacology · 2012Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ataxia-telangiectasia is a multifaceted syndrome caused by null mutations in the ATM gene, which encodes the protein kinase ATM, a key participant in the DNA damage response. Retinal neurons are highly susceptible to DNA damage because they are terminally differentiated and have the highest metabolic activity in the central nervous system. In this study, we characterized the retina in young and aged Atm-deficient mice (Atm(-/-)). At 2 months of age, angiography revealed faint retinal vasculature in Atm(-/-) animals relative to wild-type controls. This finding was accompanied by increased expression of vascular endothelial growth factor protein and mRNA. Fibrinogen, generally absent from wild-type retinal tissue, was evident in Atm(-/-) retinas, whereas mRNA of the tight junction protein occludin was significantly decreased. Immunohistochemistry labeling for occludin in 6-month-old mice showed that this decrease persists in advanced stages of the disease. Concurrently, we noticed vascular leakage in Atm(-/-) retinas. Labeling for glial fibrillary acidic protein demonstrated morphological alterations in glial cells in Atm(-/-) retinas. Electroretinographic examination revealed amplitude aberrations in 2-month-old Atm(-/-) mice, which progressed to significant functional deficits in the older mice. These results suggest that impaired vascularization and astrocyte-endothelial cell interactions in the central nervous system play an important role in the etiology of ataxia-telangiectasia and that vascular abnormalities may underlie or aggravate neurodegeneration.
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