The DOI matches its Crossref record; 61 of the 61 references it cites were found in a registry or an index.
TNF primes endothelial cells for angiogenic sprouting by inducing a tip cell phenotype
Open accessAbstract
Pathological angiogenesis associated with wound healing often occurs subsequent to an inflammatory response that includes the secretion of cytokines such as tumor necrosis factor (TNF). Controversy exists on the angiogenic actions of TNF, with it being generally proangiogenic in vivo, but antiangiogenic in vitro. We find that whereas continuous administration of TNF in vitro or in vivo inhibits angiogenic sprouting, a 2- to 3-day pulse stimulates angiogenesis by inducing an endothelial “tip cell” phenotype. TNF induces the known tip cell genes platelet-derived growth factor B (PDGFB) and vascular endothelial cell growth factor receptor-2 (VEGFR2), while at the same time blocking signaling through VEGFR2, thus delaying the VEGF-driven angiogenic response. Notch signaling regulates tip cell function, and we find that TNF also induces the notch ligand jagged-1, through an NFκB-dependent mechanism. Enrichment of jagged-1 in tip cells was confirmed by immunofluorescent staining as well as by laser capture microdissection/quantitative reverse-transcription–polymerase chain reaction (qRT-PCR) of tip cells sprouting in vitro. Thus, in angiogenesis, the temporal expression of TNF is critical: it delays angiogenesis initially by blocking signaling through VEGFR2, but in addition by inducing a tip cell phenotype through an NFκB-dependent pathway, it concomitantly primes endothelial cells (ECs) for sprouting once the initial inflammatory wave has passed.
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Cites
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Mechanisms of angiogenesis and arteriogenesis
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VEGF guides angiogenic sprouting utilizing endothelial tip cell filopodia
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Points of control in inflammation
Nathan, C. (2002) · Nature · doi:10.1038/nature01320 · Cited by 2,738
Notch signalling: a simple pathway becomes complex
Bray, S. J. (2006) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2009 · Cited by 2,620
Tumor necrosis factor signaling
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Dll4 signalling through Notch1 regulates formation of tip cells during angiogenesis
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Cited by
The role of macrophage phenotype in vascularization of tissue engineering scaffolds
Spiller, K. L., Anfang, R. R., Spiller, K. J., Ng, J., Nakazawa, K. R., Daulton, J. W., & Vunjak-Novakovic, G. (2014) · Biomaterials · doi:10.1016/j.biomaterials.2014.02.012 · Cited by 948
The Multifaceted Roles Neutrophils Play in the Tumor Microenvironment
Sionov, R. V., Fridlender, Z. G., & Granot, Z. (2015) · Cancer Microenvironment · doi:10.1007/s12307-014-0147-5 · Cited by 416
Trepat, X., Chen, Z., & Jacobson, K. (2012) · Comprehensive Physiology · doi:10.1002/cphy.c110012 · Cited by 406
Mechanisms of Vessel Branching: Filopodia on Endothelial Tip Cells Lead the Way
De Smet, F., Segura, I., De Bock, K., Hohensinner, P. J., & Carmeliet, P. (2009) · Arteriosclerosis, Thrombosis, and Vascular Biology · doi:10.1161/atvbaha.109.185165 · Cited by 397
Canonical and Non-Canonical Notch Ligands
D’Souza, B., Meloty-Kapella, L., & Weinmaster, G. (2010) · Current Topics in Developmental Biology · doi:10.1016/s0070-2153(10)92003-6 · Cited by 362
Metadata
- Authors
- Sainson, R. C. A., Johnston, D. A., Chu, H. C., Holderfield, M. T., Nakatsu, M. N., Crampton, S. P., Davis, J., Conn, E., & Hughes, C. C. W.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2008-05-15
- Volume
- 111
- Issue
- 10
- Pages
- 4997-5007
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W2006122359
- Cited by
- 321
- References
- 61
- FWCI
- 5.71
- Type
- journal article
- Language
- en
- Open access
- green
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- Sainson, R. C. A., Johnston, D. A., Chu, H. C., Holderfield, M. T., Nakatsu, M. N., Crampton, S. P., Davis, J., Conn, E., & Hughes, C. C. W. (2008). TNF primes endothelial cells for angiogenic sprouting by inducing a tip cell phenotype. Blood. https://doi.org/10.1182/blood-2007-08-108597
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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