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CCL11 promotes angiogenic activity by activating the PI3K/Akt pathway in HUVECs

Authors
 Jun Young Park  ;  Yeo Wool Kang  ;  Byung Young Choi  ;  Young Chul Yang  ;  Byung Pil Cho  ;  Won Gil Cho 
Citation
 Journal of Receptors and Signal Transduction, Vol.37(4) : 416-421, 2017 
Journal Title
 Journal of Receptors and Signal Transduction 
ISSN
 1079-9893 
Issue Date
2017
MeSH
Animals ; Cell Movement/genetics ; Cell Proliferation/genetics ; Chemokine CCL11/genetics* ; Chemokine CCL11/metabolism ; Endothelial Cells/metabolism ; Gene Expression Regulation, Developmental/genetics ; Human Umbilical Vein Endothelial Cells ; Humans ; MAP Kinase Signaling System/genetics ; Neovascularization, Physiologic/genetics* ; Phosphatidylinositol 3-Kinases/genetics ; Proto-Oncogene Proteins c-akt/genetics* ; RNA, Small Interfering/genetics ; Rats ; Receptors, CCR3/genetics* ; Receptors, CCR3/metabolism ; Vascular Endothelial Growth Factor A/genetics ; Wound Healing/genetics
Keywords
CCL11 ; CCR3 ; HUVECs ; angiogenesis ; signaling pathway
Abstract
CCR3, the receptor for CCL11, is expressed on the surface of immune cells and even on non-immune cells. CCL11-CCR3 interactions can promote cell migration and proliferation. In this study, we investigated the effect of CCL11 on angiogenesis in HUVECs and also examined the molecular mechanisms of this process. We found that CCL11 induced mRNA transcription and protein expression of CCR3 in HUVECs. Moreover, the scratch wound healing assay and MTS proliferation assay both demonstrated that CCL11 promotes endothelial cell migration and induces weak proliferation. CCL11 directly induced microvessel sprouting from the rat aortic ring; these effects occurred earlier and to a greater extent than with VEGF stimulation. Furthermore, CCL11-induced phosphorylation of Akt was abolished by PI3K inhibitors. siRNA-mediated knockdown of CCR3 led to a significant reduction of PI3K phosphorylation. However, the phosphorylation levels of ERK1/2 were not changed, even after CCL11 treatment. Cumulatively, our data suggest that the CCL11-CCR3 interaction mainly activates PI3K/Akt signal transduction pathway in HUVECs.
URI
http://ir.ymlib.yonsei.ac.kr/handle/22282913/160871
DOI
10.1080/10799893.2017.1298132
Appears in Collections:
1. Journal Papers (연구논문) > 6. Others (기타) > Others
Yonsei Authors
박준영(Park, Jun Young)
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Full Text
https://www.tandfonline.com/doi/full/10.1080/10799893.2017.1298132
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