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

Journal Article · · Biochemical and Biophysical Research Communications
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  1. Graduate School of Biotechnology, College of Life Science, Kyung Hee University, 1 Seocheon-Ri Giheung-Eup, Yongin 446-701 (Korea, Republic of)
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/Flk-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.
OSTI ID:
22199667
Journal Information:
Biochemical and Biophysical Research Communications, Journal Name: Biochemical and Biophysical Research Communications Journal Issue: 1 Vol. 382; ISSN 0006-291X; ISSN BBRCA9
Country of Publication:
United States
Language:
English

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