ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2008
An Adam15 amplification loop promotes vascular endothelial growth factor-induced ocular neovascularization.
Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Developmental diversity and unique sensitivity to injury of lung endothelial subtypes during postnatal growth.iScience · 2023Article
- Identifying Novel Genes and Variants in Immune and Coagulation Pathways Associated with Macular Degeneration.Ophthalmology science · 2023Article
- ADAM and ADAMTS disintegrin and metalloproteinases as major factors and molecular targets in vascular malfunction and disease.Advances in pharmacology (San Diego, Calif.) · 2022Article
- Contribution of ADAM17 and related ADAMs in cardiovascular diseases.Cellular and molecular life sciences : CMLS · 2021Review
- ADAM (a Disintegrin and Metalloproteinase) 15 Deficiency Exacerbates Ang II (Angiotensin II)-Induced Aortic Remodeling Leading to Abdominal Aortic Aneurysm.Arteriosclerosis, thrombosis, and vascular biology · 2020Article
- Fabrication of plumbagin on silver nanoframework for tunable redox modulation: Implications for therapeutic angiogenesis.Journal of cellular physiology · 2019Article
- A Disintegrin and Metalloproteinase (ADAM) and ADAM with thrombospondin motifs (ADAMTS) family in vascular biology and disease.Biochemical pharmacology · 2019Review
- Integrating predicted transcriptome from multiple tissues improves association detection.PLoS genetics · 2019Article
- Identification of different macrophage subpopulations with distinct activities in a mouse model of oxygen-induced retinopathy.International journal of molecular medicine · 2017Article
- ADAM15 Is Functionally Associated with the Metastatic Progression of Human Bladder Cancer.PloS one · 2016Article
- Characterization of oxygen-induced retinopathy in mice carrying an inactivating point mutation in the catalytic site of ADAM15.Investigative ophthalmology & visual science · 2014Article
- Interleukin-18 has antipermeablity and antiangiogenic activities in the eye: reciprocal suppression with VEGF.Journal of cellular physiology · 2014Article
- MicroRNA-147b regulates vascular endothelial barrier function by targeting ADAM15 expression.PloS one · 2014Article
- Agents that bind annexin A2 suppress ocular neovascularization.Journal of cellular physiology · 2010Article
- Gene hunting of the Genetic Analysis Workshop 16 rheumatoid arthritis data using rough set theory.BMC proceedings · 2009Article
- Mediators of ocular angiogenesis.Journal of genetics · 2009Review
- ADAM9 is involved in pathological retinal neovascularization.Molecular and cellular biology · 2009Article
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 3 countries.
Funding
Abstract
Proteins with a disintegrin and a metalloproteinase domain (ADAMs) are a family of membrane-bound proteinases that bind integrins through their disintegrin domain. In this study, we have found modest expression of ADAM15 in pericytes in normal retina and strong up-regulation of ADAM15 in retinal vascular endothelial cells in ischemic retina. Increased expression of vascular endothelial growth factor (VEGF) in the retina in the absence of ischemia also increased ADAM15 levels, and knockdown of Vegf mRNA in ischemic retina reduced Adam15 mRNA. Mice deficient in ADAM15 showed a significant reduction in ischemia-induced retinal neovascularization, choroidal neovascularization at rupture sites in Bruch's membrane, and VEGF-induced subretinal neovascularization. ADAM15-deficient mice also showed reduced levels of VEGF(164), VEGF receptor 1, and VEGF receptor 2 in ischemic retina. These data suggest that ADAM15 and VEGF participate in an amplification loop; VEGF increases expression of ADAM15, which in turn increases expression of VEGF and its receptors. Perturbation of the loop by elimination of ADAM15 suppresses ocular neovascularization in 3 different model systems, and thus ADAM15 provides a new therapeutic target for diseases complicated by neovascularization.
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Registered trials
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