CCL23 up-regulates expression of KDR/Flk-1 and potentiates VEGF-induced proliferation and migration of human endothelial cells

被引：27

作者：

Han, Kyu Yeon ^{[1
]}

Kim, Chan Woo ^{[1
]}

Lee, Tae Hoon ^{[1
]}

Son, Youngsook ^{[1
]}

Kim, Jiyoung ^{[1
]}

机构：

[1] Kyung Hee Univ, Grad Sch Biotechnol, Coll Life Sci, Yongin 446701, South Korea

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2009年 / 382卷 / 01期

关键词：

CCL23; KDR/Flk-1; VEGF; Endothelial cells; Angiogenesis; GROWTH-FACTOR RECEPTOR-2; CC-CHEMOKINE CCL23; TYROSINE KINASE; IN-VITRO; ANGIOGENESIS; VASCULOGENESIS; PERMEABILITY; ACTIVATION; CK-BETA-8; MONOCYTES;

D O I：

10.1016/j.bbrc.2009.02.149

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

CCL23 is a CC chemokine and exerts its biological activities on endothelial cells as well as on immune cells through CCR1. We investigated the potential effect of CCL23 on expression of KDR/Flk-1 receptor in endothelial cells. PCR, confocal microscope and Western blot analysis revealed that CCL23 up-regulated KDR/Flk-1 mRNA and protein levels in endothelial cells. A reporter assay indicated that CCL23-induced KDR/Flk-1 expression primarily occurred at the transcriptional level. In addition, CCL23 stimulated phosphorylation of SAPK/JNK, and an inhibitor of SAPK/JNK blocks the CCL23-induced KDR/FIk-1 expression. Furthermore, VEGF-induced ERK phosphorylation was stimulated by CCL23. Finally, CCL23 promoted VEGF-induced endothelial proliferation and migration, which were correlated with the maximal Stimulation of KDR/Flk-1 expression by CCL23. Taken together, these findings suggest that CCL23 results in up-regulation of KDR/flk-1 receptor gene transcription and protein expression and that KDR/Flk-1 up-regulation induced by CCL23 may contribute to potentiation of VEGF action in angiogenesis. (C) 2009 Elsevier Inc. All rights reserved.

引用

页码：124 / 128

页数：5

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