The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Involvement of RhoA/Rho Kinase Signaling in VEGF-Induced Endothelial Cell Migration and Angiogenesis In Vitro
Abstract
Objective— Growth factor-induced angiogenesis involves migration of endothelial cells (ECs) into perivascular areas and requires active remodeling of the endothelial F-actin cytoskeleton. The small GTPase RhoA previously has been implicated in vascular endothelial growth factor (VEGF)-induced signaling pathways, but its role has not been clarified. Methods and Results— VEGF induced the activation of RhoA and recruited RhoA to the cell membrane of human ECs. This increase in RhoA activity is necessary for the VEGF-induced reorganization of the F-actin cytoskeleton, as demonstrated by adenoviral transfection of dominant-negative RhoA. Rho kinase mediated this effect of RhoA, as was demonstrated by the use of Y-27632, a specific inhibitor of Rho kinase. Inhibition of Rho kinase prevented the VEGF-enhanced EC migration in response to mechanical wounding but had no effect on basal EC migration. Furthermore, in an in vitro model for angiogenesis, inhibition of either RhoA or Rho kinase attenuated the VEGF-mediated ingrowth of ECs in a 3-dimensional fibrin matrix. Conclusions— VEGF-induced cytoskeletal changes in ECs require RhoA and Rho kinase, and activation of RhoA/Rho kinase signaling is involved in the VEGF-induced in vitro EC migration and angiogenesis.
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GEF-H1 is involved in agonist-induced human pulmonary endothelial barrier dysfunction
Birukova, A. A., Adyshev, D., Gorshkov, B., Bokoch, G. M., Birukov, K. G., & Verin, A. D. (2006) · American Journal of Physiology-Lung Cellular and Molecular Physiology · doi:10.1152/ajplung.00259.2005 · Cited by 173
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STAT3-YAP/TAZ signaling in endothelial cells promotes tumor angiogenesis
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Metadata
- Authors
- van Nieuw Amerongen, G. P., Koolwijk, P., Versteilen, A., & van Hinsbergh, V. W. M.
- Venue
- Arteriosclerosis, Thrombosis, and Vascular Biology
- Published
- 2003-02
- Volume
- 23
- Issue
- 2
- Pages
- 211-217
- ISSN
- 1079-5642 (ISSN-L)
- 1524-4636
- OpenAlex
- W2164321835
- Cited by
- 329
- References
- 52
- FWCI
- 5.36
- Type
- journal article
- Language
- en
- Open access
- closed
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