期刊
FEBS LETTERS
卷 585, 期 1, 页码 159-166出版社
WILEY
DOI: 10.1016/j.febslet.2010.11.031
关键词
Neutrophil; Inflammation; Proleukemic cell; Janus kinase 3; Kinase; Flavonoid
资金
- National Institutes of Health [HL056653]
- NHLBI [NHLBI-HL 075040]
Janus kinase 3 (JAK3) is a non-receptor tyrosine kinase vital to the regulation of T-cells. We report that JAK3 is a mediator of interleukin-8 (IL-8) stimulation of a different class of hematopoietic relevant cells: human neutrophils. IL-8 induced a time- and concentration-dependent activation of JAK3 activity in neutrophils and differentiated HL-60 leukemic cells. JAK3 was more robustly activated by IL-8 than other kinases: p70S6K, mTOR, MAPK or PKC. JAK3 silencing severely inhibited IL-8-mediated chemotaxis. Thus, IL-8 stimulates chemotaxis through a mechanism mediated by JAK3. Further, JAK3 activity and chemotaxis were inhibited by the flavonoid apigenin (40,5,7-trihydroxyflavone) at similar to 5 nM IC50. These new findings lay the basis for understanding the molecular mechanism of cell migration as it relates to neutrophil-mediated chronic inflammatory processes. (C) 2010 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.
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