Leukotactin-1/CCL15 induces cell migration and differentiation of human eosinophilic leukemia EoL-1 cells through PKCδ activation |
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Authors: | Ji-Sook Lee In Sik Kim |
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Institution: | (1) Department of Biology, College of Natural Sciences, Daejeon University, Daejeon, 300-716, Republic of Korea;(2) Department of Biomedical Laboratory Science, School of Medicine, Eulji University, 143-5, Yeuongdu-dong, Jung-gu, Daejeon, 301-746, Republic of Korea; |
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Abstract: | Leukotactin-1 (Lkn-1)/CCL15 is a CC chemokine that binds to the CCR1 and CCR3. Lkn-1 functions as an essential factor in the
migration of monocytes, lymphocytes, and neutrophils. Although eosinophils express both receptors, the role of Lkn-1 in immature
eosinophils remains to be elucidated. In this present study, we investigated the contribution of the CCR1-binding chemokines
to chemotactic activity and in the differentiation in the human eosinophilic leukemia cell line EoL-1. Lkn-1 induced the stronger
migration of EoL-1 cells than other CCR1-binding chemokines such as RANTES/CCL5, MIP-1α/CCL3 and HCC-4/CCL16. Lkn-1-induced
chemotaxis was inhibited by pertussis toxin, an inhibitor of Gi/Go protein; U73122, an inhibitor of phospholipase C and rottlerin, an inhibitor of protein kinase C delta (PKCδ). Lkn-1 increased
PKCδ activity, which was partially blocked by the pertussis toxin and U73122. Lkn-1 enhanced the butyric acid-induced differentiation
via PKCδ after binding to the increased CCR1 because Lkn-1 caused EoL-1 cells to change morphologically into mature eosinophil-like
cells. Likewise, Lkn-1 increased the expression of both eosinophil peroxidase (EPO) and the major basic protein (MBP). PKCδ
activation due to Lkn-1 is involved in migration, as well as the butyric acid-induced differentiation. This finding contributes
to an understanding of CC chemokines in eosinophil biology and to the development of novel therapies for the treatment of
eosinophilic disorders. This study suggests the pivotal roles of Lkn-1 in the regulation of the movement and development of
eosinophils. |
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