ArticleOncogene2001
Two distinct signalling pathways are involved in FGF2-stimulated proliferation of choriocapillary endothelial cells: a comparative study with VEGF.
Article in Oncogene, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 85 citations in OpenAlex.
- Loss of mitochondrial DNA helicase in retinal macroglia drives neovascular retinopathy.EMBO molecular medicine · 2026Article
- Elucidating glial responses to products of diabetes-associated systemic dyshomeostasis.Progress in retinal and eye research · 2023Review
- Key Role of Astrocytes in Postnatal Brain and Retinal Angiogenesis.International journal of molecular sciences · 2022Review
- Long Noncoding RNAInternational journal of molecular sciences · 2021Article
- The Vitreous Ecosystem in Diabetic Retinopathy: Insight into the Patho-Mechanisms of Disease.International journal of molecular sciences · 2021Review
- Article
- Effect of luteolin on apoptosis and vascular endothelial growth factor in human choroidal melanoma cells.International journal of ophthalmology · 2021Article
- Review
- FGF family members differentially regulate maturation and proliferation of stem cell-derived astrocytes.Scientific reports · 2019Article
- The Histone Deacetylase Inhibitor AN7, Attenuates Choroidal Neovascularization in a Mouse Model.International journal of molecular sciences · 2019Article
- Mosaic-variegated aneuploidy syndrome mutation or haploinsufficiency in Cep57 impairs tumor suppression.The Journal of clinical investigation · 2018Article
- Establishment of a three-dimensional model to study human uterine angiogenesis.Molecular human reproduction · 2018Article
- High molecular weight FGF2 isoforms demonstrate canonical receptor-mediated activity and support human embryonic stem cell self-renewal.Stem cell research · 2017Article
- Retinal and choroidal angiogenesis: a review of new targets.International journal of retina and vitreous · 2017Review
- Modulation of unloading-induced bone loss in mice with altered ERK signaling.Mammalian genome : official journal of the International Mammalian Genome Society · 2016Article
- Establishment of neutralizing rat monoclonal antibodies for fibroblast growth factor-2.Monoclonal antibodies in immunodiagnosis and immunotherapy · 2014Article
- Expression of thrombospondin-1 modulates the angioinflammatory phenotype of choroidal endothelial cells.PloS one · 2014Article
- Article
- Bevacizumab inhibits proliferation of choroidal endothelial cells by regulation of the cell cycle.Clinical ophthalmology (Auckland, N.Z.) · 2013Article
- Short-term efficacy of intravitreal dobesilate in central serous chorioretinopathy.European journal of medical research · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the retina, angiogenesis is an important component of normal physiological events such as embryonic vascular development. It is also involved in pathological processes including diabetic retinopathies and age-related macular degeneration, and tumour growth such as choroidal melanoma. Fibroblast growth factor (FGF) 2 and vascular endothelial cell growth factor (VEGF) are the two major angiogenic factors in the retina. We investigated the mechanism of proliferation and the regulation of the mitogenic properties of FGF2 and VEGF in cultures of chorocapillary endothelial cells (CEC). FGF2 is a strong mitogen for CEC and induced a 2.5-fold increase in cell proliferation after 4 days in culture in the absence of serum. In contrast, VEGF is a poor mitogen for CEC. FGF2, but not VEGF induces a large activation of MEK1, ERK1/2 and P90(RSK) during CEC proliferation. Pharmacological inhibition of Ras processing, and of MEK1 and ERK1/2 activation reduced only by 50% FGF2-induced cell proliferation, suggesting that there is another signalling pathway for CEC proliferation. Pharmacological inhibition of the PI 3-Kinase also inhibits by half FGF2-induced CEC proliferation. FGF2 stimulates the activation of the PI 3-K, P70(S6K) and Akt. Inhibition of both ERK1/2 and PI 3-K activities suppressed FGF2-induced CEC proliferation, demonstrating that CEC proliferation requires both ERKs and PI 3-K pathways. These data on the molecular mechanism and signalling may have important implications for providing more selective methods for anti-angiogenic and anti-tumoural therapy.
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Registered trials
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.