ArticleMolecular vision2008
Overexpression of a mutant form of TGFBI/BIGH3 induces retinal degeneration in transgenic mice.
Article in Molecular vision, 2008. 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, 25 citations in OpenAlex.
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- IC100, a humanized therapeutic monoclonal anti-ASC antibody alleviates oxygen-induced retinopathy in mice.Angiogenesis · 2024Article
- Functions of Matricellular Proteins in Dental Tissues and Their Emerging Roles in Orofacial Tissue Development, Maintenance, and Disease.International journal of molecular sciences · 2021Review
- Effect of osmolytes on in-vitro aggregation properties of peptides derived from TGFBIp.Scientific reports · 2020Article
- Identification of a Heterozygous Mutation in theJournal of ophthalmology · 2019Article
- Genetics in Keratoconus: where are we?Eye and vision (London, England) · 2016Review
- The role of novel and known extracellular matrix and adhesion molecules in the homeostatic and regenerative bone marrow microenvironment.Cell adhesion & migration · 2014Review
- Construction of eukaryotic plasmid expressing human TGFBI and its influence on human corneal epithelial cells.International journal of ophthalmology · 2012Article
- TGFB1-induced extracellular expression of TGFBIp and inhibition of TGFBIp expression by RNA interference in a human corneal epithelial cell line.Investigative ophthalmology & visual science · 2011Article
- TGFBI deficiency predisposes mice to spontaneous tumor development.Cancer research · 2009Article
- Abnormal regulation of extracellular matrix and adhesion molecules in corneas of patients with keratoconus.International journal of keratoconus and ectatic corneal diseasesArticle
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeDespite ubiquitous expression of the keratoepithelin (KE) protein encoded by the transforming growth factor beta induced/beta induced gene human clone 3 (TGFBI/BIGH3) gene, corneal dystrophies are restricted to the cornea, and no other tissues are affected. We investigated the role of TGFBI/BIGH3 in Groenouw corneal dystrophies by generating transgenic mice overexpressing TGFBI/BIGH3 containing the R555W mutation.
methodsTransgenic animals expressing the Groenouw mutation of human TGFBI/BIGH3 were generated using lentiviral vectors. The line expressed TGFBI/BIGH3 containing the R555W mutation under the control of the phosphoglycerate kinase (PGK) promoter. Expression of the transgene was monitored by Southern and western blotting and by RT-PCR. Electroretinogram analysis was performed and four mice were subjected to complete necroscopy.
resultsTransgene expression was observed in different organs although without specific expression in the cornea. The overall morphology of the transgenic animals was not severely affected by KE overexpression. However, we observed an age-dependent retinal degeneration both functionally and histologically. Female-specific follicular hyperplasia in the spleen and increased levels of lipofuscin in the adrenal gland were also seen in transgenic animals.
conclusionsCellular degeneration in the retina of transgenic animals suggest that perturbation of the transforming growth factor beta (TGFbeta) family regulation may affect photoreceptor survival and may induce possible accelerated aging in several tissues. No corneal phenotype could be observed, probably due to the lack of transgene expression in this tissue.
Indexed as
Identifiers
18568131PMC2429980W2016574126What OpenQuestion holds
Registered trials
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