ArticleThe American journal of pathology2007
Tumoral and choroidal vascularization: differential cellular mechanisms involving plasminogen activator inhibitor type I.
Article in The American journal of pathology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Consensus guidelines for the use and interpretation of angiogenesis assays.Angiogenesis · 2018Review
- Bone marrow-derived cells in ocular neovascularization: contribution and mechanisms.Angiogenesis · 2016Review
- Optimization of an Image-Guided Laser-Induced Choroidal Neovascularization Model in Mice.PloS one · 2015Article
- Laser-induced choroidal neovascularization model to study age-related macular degeneration in mice.Nature protocols · 2013Article
- Myopia and inflammation.Journal of ophthalmic & vision research · 2011Article
- Bone marrow-derived mesenchymal cells and MMP13 contribute to experimental choroidal neovascularization.Cellular and molecular life sciences : CMLS · 2011Article
- Article
- Article
- Plasminogen activator inhibitor-1 (PAI-1) facilitates retinal angiogenesis in a model of oxygen-induced retinopathy.Investigative ophthalmology & visual science · 2009Article
- ETS-1 and ETS-2 are upregulated in a transgenic mouse model of pigmented ocular neoplasm.Molecular vision · 2008Article
Corrections and comments
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Authors and funding
19 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
An adequate balance between serine proteases and their plasminogen activator inhibitor-1 (PAI-1) is critical for pathological angiogenesis. PAI-1 deficiency in mice is associated with impaired choroidal neovascularization (CNV) and tumoral angiogenesis. In the present work, we demonstrate unexpected differences in the contribution of bone marrow (BM)-derived cells in these two processes regulated by PAI-1. PAI-1(-/-) mice grafted with BM-derived from wild-type mice were able to support laser-induced CNV formation but not skin carcinoma vascularization. Engraftment of irradiated wild-type mice with PAI-1(-/-) BM prevented CNV formation, demonstrating the crucial role of PAI-1 delivered by BM-derived cells. In contrast, the transient infiltration of tumor transplants by local PAI-1-producing host cells rather than by BM cells was sufficient to rescue tumor growth and angiogenesis in PAI-1-deficient mice. These data identify PAI-1 as a molecular determinant of a local permissive soil for tumor angiogenesis. Altogether, the present study demonstrates that different cellular mechanisms contribute to PAI-1-regulated tumoral and CNV. PAI-1 contributes to BM-dependent choroidal vascularization and to BM-independent tumor growth and angiogenesis.
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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.