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Suh, Pann-Ghill
BioSignal Network Lab (BSN)
Research Interests
  • Signal transduction, cancer, metabolism, phospholipase C

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Functional interaction between CTGF and FPRL1 regulates VEGF-A-induced angiogenesis

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Title
Functional interaction between CTGF and FPRL1 regulates VEGF-A-induced angiogenesis
Author
Lee, Mi-SookGhim, JaewangKim, Sun-JinYun, Young SungYoo, Seung-AhSuh, Pann-GhillKim, Wan-UkRyu, Sung Ho
Issue Date
2015-07
Publisher
ELSEVIER SCIENCE INC
Citation
CELLULAR SIGNALLING, v.27, no.7, pp.1439 - 1448
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
URI
https://scholarworks.unist.ac.kr/handle/201301/16404
URL
http://www.sciencedirect.com/science/article/pii/S0898656815001266
DOI
10.1016/j.cellsig.2015.04.001
ISSN
0898-6568
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