Autocrine VEGF signaling is required for vascular homeostasis.

By Sunyoung Lee, Tom T. Chen, Chad L. Barber, M. Jordan, J. Murdock, S. Desai, N. Ferrara, A. Nagy, Kenneth P. Roos, M. Luisa Iruela-Arispe. Cell, 2007

1,080 citations recorded by the source corpus.

Subfields: Cancer Research, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/a553f74774ea2c8ccec20199e914c31785fbb120

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Citations in the corpus

Vascular Endothelial Growth Factor (VEGF) and Its Receptor (VEGFR) Signaling in Angiogenesis: A Crucial Target for Anti- and Pro-Angiogenic Therapies. (2011, background): “showed that an autocrine loop of VEGF-A and its receptor system exist within vascular endothelial cells, contributing to endothelial functions.(15)”
Signal transduction by vascular endothelial growth factor receptors. (2012, background): “Analyses of recombinant mice specifically lacking EC-produced VEGF indicate that paracrine VEGF may not compensate for autocrine VEGF (Lee et al. 2007).”
Endogenous VEGF Is Required for Visual Function: Evidence for a Survival Role on Müller Cells and Photoreceptors (2008, background): “observed in many tumor cells [46,47] but only in a few normal cell types, such as podocytes [48], skeletal muscle [49], aortic endothelium [50,51], and RPE [3].”
Control of vascular morphogenesis and homeostasis through the angiopoietin–Tie system (2009, background): “Intriguingly, these experiments also suggested that EC-derived ANG2 might act through an internal autocrine-loop mechanism, which is also called intracrine signalling, similar to the role of autocrine, EC-derived VEGF in controlling vascular homeostasi”
Macrophage-Induced Blood Vessels Guide Schwann Cell-Mediated Regeneration of Peripheral Nerves (2015, background): “Macrophages have been shown to promote angiogenesis (Fantin et al., 2010; Pollard, 2009) and autocrine VEGF-A signaling helps to maintain the health of ECs (Lee et al., 2007).”
Role of platelet-derived growth factors in physiology and medicine. (2008, positive): “(Lee et al. 2007), have not been demonstrated for the PDGFs.”
Anti-angiogenic therapy for cancer: current progress, unresolved questions and future directions (2014, background): “These include: endothelial cells of the normal vasculature [218], dendritic cells [219], myeloid cells [220], neurons [221], pericytes [222] and tumour cells [201, 212, 223–228].”
Molecular mechanisms and clinical applications of angiogenesis (2011, background): “, whereas autocrine VEGF, released by endothelial cells, maintains vascular homeostasi”
The roles of vascular endothelial growth factor in bone repair and regeneration (2016, background): “This phenomenon was first reported based on studies of VEGF signaling in the survival of hematopoietic and endothelial cells [107, 108].”
Endothelial expression of autocrine VEGF upon the uptake of tumor-derived microvesicles containing oncogenic EGFR (2009, background): “Interestingly, VEGF was recently found to be expressed by endothelial cells, where it plays an important homeostatic role (22).”
Targeting the tumour vasculature: insights from physiological angiogenesis (2010, positive): “However, this distinction is not absolute as previous studies have indicated that autocrine VEGFA signalling also has some role in normal vascular homeostasis and haematopoietic stem cell surviva”
The blood-brain barrier. (2015, background): “During early embryogenesis, radial glia cells seem to be the source of VEGF needed for vascular development, although ECs have been described to promote cell-autonomous activation of the VEGF signaling (Lee et al. 2007).”
Endothelial adherens junctions control tight junctions by VE-cadherin-mediated upregulation of claudin-5 (2008, background): “It has been reported that ECs are able to express VEGF-A endogenousl”
Engraftment and reconstitution of hematopoiesis is dependent on VEGFR2 mediated regeneration of sinusoidal endothelial cells (2009, positive): “that demonstrates the constitutive deletion of VEGF-A autocrine signaling in surviving adult mice manifested no apparent hematological defects (Lee et al., 2007).”