ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2010
The melanoma-associated transmembrane glycoprotein Gpnmb controls trafficking of cellular debris for degradation and is essential for tissue repair.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers, 1 of them a synthesis that pooled it.
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Who cites it
88 citing papers in PubMed, 1 synthesis or guideline pooled it, 143 citations in OpenAlex.
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- Plasticity of human microglia and brain perivascular macrophages in aging and Alzheimer's disease.Nature genetics · 2026Article
- Single-cell atlas of the mouse ovary reveals molecular drivers of aging and senescence during the estropausal transition.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Gpnmb defines a phagocytic state of microglia linked to cell death in prion disease mouse model.Nature communications · 2026Article
- Osteoactivin/GPNMB as a candidate biomarker of diabetic nephropathy in type 2 diabetes: associations with angiogenic and kidney injury biomarkers.Frontiers in endocrinology · 2026Article
- Regulation of lipoprotein processing by GPNMB in foamy macrophages: potential therapeutic targets for atherosclerosis.Nature communications · 2025Article
- Article
- Single-cell spatial transcriptomics unravels the cellular landscape of abdominal aortic aneurysm.JCI insight · 2025Article
- Bidirectional regulation of glycoprotein nonmetastatic melanoma protein B by β-glucocerebrosidase deficiency inbioRxiv : the preprint server for biology · 2025Article
- Multinucleated giant cells are hallmarks of ovarian aging with unique immune and degradation-associated molecular signatures.PLoS biology · 2025Article
- Malignant mesothelioma-associated inflammatory microenvironment promotes tumor progression via GPNMB.Journal of translational medicine · 2025Article
- Galectin-3: a novel biomarker of glycogen storage disease type III.Cell death discovery · 2025Article
- A novel uORF regulates folliculin to promote cell growth and lysosomal biogenesis during cardiac stress.Scientific reports · 2025Article
- Identification of GPNMB in endometrial cancer based on pan-cancer analysis and in vitro validation.Discover oncology · 2024Article
- Spatiotemporal transcriptomic mapping of regenerative inflammation in skeletal muscle reveals a dynamic multilayered tissue architecture.The Journal of clinical investigation · 2024Article
- Regional Differences in the Small Intestinal Proteome of Control Mice and of Mice Lacking Lysosomal Acid Lipase.Journal of proteome research · 2024Article
- Investigating the role and regulation of GPNMB in progranulin-deficient macrophages.Frontiers in immunology · 2024Article
- Glycoprotein Non-Metastatic Protein B (GPNMB): The Missing Link Between Lysosomes and Obesity.Experimental and clinical endocrinology & diabetes : official journal, German Society of Endocrinology [and] German Diabetes Association · 2023Review
- Progranulin and GPNMB: interactions in endo-lysosome function and inflammation in neurodegenerative disease.Journal of neuroinflammation · 2023Review
28 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Kidney damage due to injury rarely resolves completely, and there are currently no therapies capable of promoting repair. In addition to understanding mechanisms by which tissues are damaged, illuminating mechanisms of repair and regeneration is also of great importance. Here we show that the melanoma-associated, transmembrane glycoprotein, Gpnmb, is up-regulated 15-fold following ischemic damage in kidney tissue and by more than 10-fold in macrophages and 3-fold in surviving epithelial cells. Gpnmb-expressing macrophages and epithelial cells were found to contain apoptotic bodies at 3 times the rate of nonexpressing cells. Either mutation of Gpnmb or ablation of inflammatory macrophages prevents normal repair of the kidney. Significantly, the kidneys from postischemic Gpnmb mutant mice exhibited a 5-fold increase in apoptotic cellular debris compared to wild-type mice. These mice also experienced an 85% increase in mortality following bilateral ischemic kidney. Finally, we demonstrate that Gpnmb is a phagocytic protein that is necessary for recruitment of the autophagy protein LC3 to the phagosome where these proteins are colocalized and for lysosomal fusion with the phagosome and hence bulk degradation of their content. Therefore, Gpnmb is a novel prorepair gene that is necessary for crosstalk between the macroautophagic degradation pathway and phagocytosis.
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Registered trials
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