ArticleThe Journal of biological chemistry2008
A novel role of vascular endothelial cadherin in modulating c-Src activation and downstream signaling of vascular endothelial growth factor.
Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 60 citations in OpenAlex.
- SHP2 is essential for the progesterone-promoted proliferation and migration in breast cancer cell lines.Frontiers in endocrinology · 2025Article
- Role of c-Src and reactive oxygen species in cardiovascular diseases.Molecular genetics and genomics : MGG · 2023Review
- A JAM-A-tetraspanin-αvβ5 integrin complex regulates contact inhibition of locomotion.The Journal of cell biology · 2022Article
- Expression Profile of CD157 Reveals Functional Heterogeneity of Capillaries in Human Dermal Skin.Biomedicines · 2022Article
- Vascular permeability in retinopathy is regulated by VEGFR2 Y949 signaling to VE-cadherin.eLife · 2020Article
- Growth Factor Deregulation and Emerging Role of Phosphatases in Diabetic Peripheral Artery Disease.Frontiers in cardiovascular medicine · 2020Review
- VE-cadherin regulates migration inhibitory factor synthesis and release.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- Electroacupuncture facilitates implantation by enhancing endometrial angiogenesis in a rat model of ovarian hyperstimulation.Biology of reproduction · 2019Article
- Modulation of long-term endothelial-barrier integrity is conditional to the cross-talk between Akt and Src signaling.Journal of cellular physiology · 2017Article
- Modulation of VEGF receptor 2 signaling by protein phosphatases.Pharmacological research · 2017Review
- Akt1 promotes stimuli-induced endothelial-barrier protection through FoxO-mediated tight-junction protein turnover.Cellular and molecular life sciences : CMLS · 2016Article
- VE-cadherin facilitates BMP-induced endothelial cell permeability and signaling.Journal of cell science · 2016Article
- Novel role of reactive oxygen species-activated Trp melastatin channel-2 in mediating angiogenesis and postischemic neovascularization.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
- Regulation of Endothelial Adherens Junctions by Tyrosine Phosphorylation.Mediators of inflammation · 2015Review
- Thioredoxin-interacting protein is a biomechanical regulator of Src activity: key role in endothelial cell stress fiber formation.Circulation research · 2014Article
- SHP-2 binds to caveolin-1 and regulates Src activity via competitive inhibition of CSK in response to H2O2 in astrocytes.PloS one · 2014Article
- The HCMV gH/gL/UL128-131 complex triggers the specific cellular activation required for efficient viral internalization into target monocytes.PLoS pathogens · 2013Article
- NHERF-2 maintains endothelial homeostasis.Blood · 2012Article
- Signaling required for blood vessel maintenance: molecular basis and pathological manifestations.International journal of vascular medicine · 2012Article
- Fibroblast growth factor signaling potentiates VE-cadherin stability at adherens junctions by regulating SHP2.PloS one · 2012Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Vascular endothelial growth factor (VEGF) is a potent mediator of angiogenesis and vascular permeability, in which c-Src tyrosine kinase plays an essential role. However, the mechanisms by which VEGF stimulates c-Src activation have remained unclear. Here, we demonstrate that vascular endothelial cadherin (VE-cadherin) plays a critical role in regulating c-Src activation in response to VEGF. In vascular endothelial cells, VE-cadherin was basally associated with c-Src and Csk (C-terminal Src kinase), a negative regulator of Src activation. VEGF stimulated Csk release from VE-cadherin by recruiting the protein tyrosine phosphatase SHP2 to VE-cadherin signaling complex, leading to an increase in c-Src activation. Silencing VE-cadherin with small interference RNA significantly reduced VEGF-stimulated c-Src activation. Disrupting the association of VE-cadherin and Csk through the reconstitution of Csk binding-defective mutant of VE-cadherin also diminished Src activation. Moreover, inhibiting SHP2 by small interference RNA and adenovirus-mediated expression of a catalytically inactive mutant of SHP2 attenuated c-Src activation by blocking the disassociation of Csk from VE-cadherin. Furthermore, VE-cadherin and SHP2 differentially regulates VEGF downstream signaling. The inhibition of c-Src, VE-cadherin, and SHP2 diminished VEGF-mediated activation of Akt and endothelial nitric-oxide synthase. In contrast, inhibiting VE-cadherin and SHP2 enhanced ERK1/2 activation in response to VEGF. These findings reveal a novel role for VE-cadherin in modulating c-Src activation in VEGF signaling, thus providing new insights into the importance of VE-cadherin in VEGF signaling and vascular function.
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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.