ArticleBMC genetics2008
GpnmbR150X allele must be present in bone marrow derived cells to mediate DBA/2J glaucoma.
Article in BMC genetics, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 46 citations in OpenAlex.
- Spatiotemporal transcriptomic mapping of regenerative inflammation in skeletal muscle reveals a dynamic multilayered tissue architecture.The Journal of clinical investigation · 2024Article
- Lack of evidence for GWAS signals of exfoliation glaucoma working via monogenic loss-of-function mutation in the nearest gene.Human molecular genetics · 2024Article
- Pigment Dispersion Contributes to Ocular Immune Privilege in a DBA/2J Mouse Model of Pigmentary Glaucoma.Investigative ophthalmology & visual science · 2024Article
- Modeling complex age-related eye disease.Progress in retinal and eye research · 2024Review
- Exploring Early-Stage Retinal Neurodegeneration in Murine Pigmentary Glaucoma: Insights From Gene Networks and miRNA Regulation Analyses.Investigative ophthalmology & visual science · 2023Article
- IGFBPL1 is a master driver of microglia homeostasis and resolution of neuroinflammation in glaucoma and brain tauopathy.Cell reports · 2023Article
- Apolipoprotein E4 impairs the response of neurodegenerative retinal microglia and prevents neuronal loss in glaucoma.Immunity · 2022Article
- Anti-inflammatory role of Gpnmb in adipose tissue of mice.Scientific reports · 2021Article
- Functional Domains and Evolutionary History of the PMEL and GPNMB Family Proteins.Molecules (Basel, Switzerland) · 2021Article
- BrdU Positive Cells Induced in a Genetic Mouse Model of Glaucoma.Journal of ophthalmology & visual sciences · 2021Article
- Complement peptide C3a receptor 1 promotes optic nerve degeneration in DBA/2J mice.Journal of neuroinflammation · 2020Article
- Glycoprotein nonmetastatic melanoma protein B: A key mediator and an emerging therapeutic target in autoimmune diseases.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Review
- Angiopoietin-1 Knockout Mice as a Genetic Model of Open-Angle Glaucoma.Translational vision science & technology · 2020Article
- Inhibition of monocyte-like cell extravasation protects from neurodegeneration in DBA/2J glaucoma.Molecular neurodegeneration · 2019Article
- Investigating a downstream gene ofMolecular vision · 2019Article
- Molecular Genetics of Pigment Dispersion Syndrome and Pigmentary Glaucoma: New Insights into Mechanisms.Journal of ophthalmology · 2018Review
- Loss of Fractalkine Signaling Exacerbates Axon Transport Dysfunction in a Chronic Model of Glaucoma.Frontiers in neuroscience · 2016Article
- Using genetic mouse models to gain insight into glaucoma: Past results and future possibilities.Experimental eye research · 2015Review
- Experimentally Induced Mammalian Models of Glaucoma.BioMed research international · 2015Review
- Determining immune components necessary for progression of pigment dispersing disease to glaucoma in DBA/2J mice.BMC genetics · 2014Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThe Gpnmb gene encodes a transmembrane protein whose function(s) remain largely unknown. Here, we assess if a mutant allele of Gpnmb confers susceptibility to glaucoma by altering immune functions. DBA/2J mice have a mutant Gpnmb gene and they develop a form of glaucoma preceded by a pigment dispersing iris disease and abnormalities of the immunosuppressive ocular microenvironment.
resultsWe find that the Gpnmb genotype of bone-marrow derived cell lineages significantly influences the iris disease and the elevation of intraocular pressure. GPNMB localizes to multiple cell types, including pigment producing cells, bone marrow derived F4/80 positive antigen-presenting cells (APCs) of the iris and dendritic cells. We show that APCs of DBA/2J mice fail to induce antigen induced immune deviation (a form of tolerance) when treated with TGFbeta2. This demonstrates that some of the immune abnormalities previously identified in DBA/2J mice result from intrinsic defects in APCs. However, the tested APC defects are not dependent on a mutant Gpnmb gene. Finally, we show that the Gpnmb mediated iris disease does not require elevated IL18 or mature B or T lymphocytes.
conclusionThese results establish a role for Gpnmb in bone marrow derived lineages. They suggest that affects of Gpnmb on innate immunity influence susceptibility to glaucoma in DBA/2J mice.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.