Genkwadaphnin promotes leukocyte migration by increasing CD44 expression via PKD1/NF-κB signaling pathway

Cited 4 time in scopus
Metadata Downloads
Title
Genkwadaphnin promotes leukocyte migration by increasing CD44 expression via PKD1/NF-κB signaling pathway
Author(s)
Nina Yoo; Ha-Reum Lee; Jang-Mi Son; Ho-Bum Kang; Hee Gu LeeSuk Ran Yoon; S Y Yoon; Jae Wha Kim
Bibliographic Citation
Immunology Letters, vol. 173, pp. 69-76
Publication Year
2016
Abstract
Genkwadaphnin (GD), an extract from the flower buds of Daphne genkwa Siebold & Zucc. (Thymelaeaceae) has been reported a significant anti-leukemic activity. However, its functional mechanism has not been defined well. To study the biological mechanism of GD function, we have investigated whether GD affects CD44 expression, which has a role in the regulation of immune cell motilities, and identified the related signaling pathways. GD treatment induced the increase of CD44 expression in a time- and concentration-dependent manner, which was specific for immune cells. GD activated PKD1/NF-κB signaling to induce CD44 expression, and resulted in the increased migration of K562 cells. In invasion assay, cell migratory ability was induced by GD and the transfection with CD44-specific short hairpin RNA resulted in reduction of its cell migration. GD treated human peripheral blood mononuclear cell (PBMC) were also shown the increased CD44 expression and migration. These data suggest that the induction of CD44 expression by GD treatment promotes immune cell transmigration resulting in the enhanced innate immunity.
Keyword
CD44GenkwadaphninLeukocyteMigrationNF-κBPKD1
ISSN
0165-2478
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.imlet.2016.03.006
Type
Article
Appears in Collections:
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
Division of Biomaterials Research > Cell Factory Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.