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DC Field | Value | Language |
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dc.citation.endPage | 1448 | - |
dc.citation.number | 7 | - |
dc.citation.startPage | 1439 | - |
dc.citation.title | CELLULAR SIGNALLING | - |
dc.citation.volume | 27 | - |
dc.contributor.author | Lee, Mi-Sook | - |
dc.contributor.author | Ghim, Jaewang | - |
dc.contributor.author | Kim, Sun-Jin | - |
dc.contributor.author | Yun, Young Sung | - |
dc.contributor.author | Yoo, Seung-Ah | - |
dc.contributor.author | Suh, Pann-Ghill | - |
dc.contributor.author | Kim, Wan-Uk | - |
dc.contributor.author | Ryu, Sung Ho | - |
dc.date.accessioned | 2023-12-22T01:07:53Z | - |
dc.date.available | 2023-12-22T01:07:53Z | - |
dc.date.created | 2015-08-17 | - |
dc.date.issued | 2015-07 | - |
dc.description.abstract | Vascular endothelial growth factor-A (VEGF-A) is a master regulator of angiogenesis that controls several angiogenic processes in endothelial cells. However, the detailed mechanisms of VEGF-A responsible for pleiotropic functions and crosstalk with other signaling pathways have not been fully understood. Here, we found that VEGF-A utilizes the connective tissue growth factor (CTGF)/formyl peptide receptor-like 1 (FPRL1) axis as one of its mediators in angiogenesis. Using a proteomic approach, we found increased secretion of a matricellular protein, CTGF, from VEGF-A-treated human umbilical vein endothelial cells (HUVECs). Then, we studied the effect of CTGF binding to FPRL1 in VEGF-A-induced angiogenesis. CTGF directly binds to FPRL1 through a linker region and activates the downstream signals of FPRL1, such as increase in extracellular signal-regulated kinase (ERK) phosphorylation and intracellular Ca2+ concentration. We found that linker region-induced FPRL1 activation promotes the migration and network formation of HUVECs, while disruption of FPRL1 inhibits VEGF-A-induced HUVEC migration and network formation. In addition, similar results were observed by the chorioallantoic membrane (CAM) assay based evaluation of angiogenesis in vivo. To summarize, our data reveal a novel working model for VEGF-A-induced angiogenesis via the VEGF-A/CTGF/FPRL1 axis that might prolong and enhance the signals initiated from VEGF-A. (C) 2015 Elsevier Inc All rights reserved | - |
dc.identifier.bibliographicCitation | CELLULAR SIGNALLING, v.27, no.7, pp.1439 - 1448 | - |
dc.identifier.doi | 10.1016/j.cellsig.2015.04.001 | - |
dc.identifier.issn | 0898-6568 | - |
dc.identifier.scopusid | 2-s2.0-84928380185 | - |
dc.identifier.uri | https://scholarworks.unist.ac.kr/handle/201301/16404 | - |
dc.identifier.url | http://www.sciencedirect.com/science/article/pii/S0898656815001266 | - |
dc.identifier.wosid | 000355887500017 | - |
dc.language | 영어 | - |
dc.publisher | ELSEVIER SCIENCE INC | - |
dc.title | Functional interaction between CTGF and FPRL1 regulates VEGF-A-induced angiogenesis | - |
dc.type | Article | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
dc.subject.keywordAuthor | Vascular endothelial growth factor-A | - |
dc.subject.keywordAuthor | Formyl peptide receptor-like 1 | - |
dc.subject.keywordAuthor | Connective tissue growth factor | - |
dc.subject.keywordAuthor | WRW4 | - |
dc.subject.keywordPlus | TISSUE GROWTH-FACTOR | - |
dc.subject.keywordPlus | FORMYL-PEPTIDE RECEPTORS | - |
dc.subject.keywordPlus | VASCULAR ENDOTHELIAL-CELLS | - |
dc.subject.keywordPlus | PROTEIN-COUPLED RECEPTORS | - |
dc.subject.keywordPlus | INTEGRIN ALPHA(V)BETA(3) | - |
dc.subject.keywordPlus | IN-VIVO | - |
dc.subject.keywordPlus | ADHESION | - |
dc.subject.keywordPlus | ACTIVATION | - |
dc.subject.keywordPlus | EXPRESSION | - |
dc.subject.keywordPlus | MIGRATION | - |
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