PMID- 19664934
OWN - NLM
STAT- MEDLINE
DCOM- 20100304
LR  - 20220309
IS  - 1096-0023 (Electronic)
IS  - 1043-4666 (Linking)
VI  - 48
IP  - 3
DP  - 2009 Dec
TI  - The roles of MCP-1 and protein kinase C delta activation in human eosinophilic 
      leukemia EoL-1 cells.
PG  - 186-95
LID - 10.1016/j.cyto.2009.07.008 [doi]
AB  - Idiopathic hypereosinophilc syndrome is a disorder associated with clonally 
      eosinophilic proliferation. The importance of FIP1-like-1-platelet-derived growth 
      factor receptor-alpha (FIP1L1-PDGFRA) in the pathogenesis and classification of 
      HES has been recently reported. In this study, we investigated the contribution 
      of monocyte chemoattractant protein-1 (MCP-1)/CCL2 to chemotactic activity and 
      protein kinase C delta (PKC delta in the human eosinophilic leukemia cell line 
      EoL-1. These cells express CCR2 protein among the CC chemokine receptors 
      (CCR1-5). MCP-1 induces strong migration of EoL-1 cells and the chemotaxis signal 
      in response to MCP-1 involves a G(i)/G(o) protein, phospholipase C (PLC), PKC 
      delta, p38 MAPK and NF-kappaB. MCP-1 activates p38 MAPK via G(i)/G(o) protein, 
      PLC and PKC delta cascade. MCP-1 also induces NF-kappaB translocation and the 
      activation is inhibited by PKC delta activation. The increase in the basal 
      expression and activity of PKC delta in EoL-1 cells, compared to normal 
      eosinophils, inhibits apoptosis in EoL-1 cells. Anti-apoptotic mechanism of PKC 
      delta is related to inhibition of caspase 3 and caspase 9, but not to 
      FIP1L1-PDGFRA. PKC delta functions as an anti-apoptotic molecule, and is involved 
      in EoL-1 cell movement stimulated by MCP-1. This study contributes to an 
      understanding of MCP-1 in eosinophil biology and pathogenic mechanism of 
      eosinophilic disorders.
FAU - Lee, Ji-Sook
AU  - Lee JS
AD  - Department of Biomedical Laboratory Science, School of Medicine, Eulji 
      University, Daejeon 301-746, Republic of Korea.
FAU - Yang, Eun Ju
AU  - Yang EJ
FAU - Kim, In Sik
AU  - Kim IS
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090806
PL  - England
TA  - Cytokine
JT  - Cytokine
JID - 9005353
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - EC 2.7.11.13 (Protein Kinase C-delta)
SB  - IM
MH  - Apoptosis
MH  - Blotting, Western
MH  - Cell Line, Tumor
MH  - Chemokine CCL2/*metabolism
MH  - Enzyme Activation
MH  - Eosinophils/enzymology/metabolism
MH  - Flow Cytometry
MH  - Humans
MH  - Hypereosinophilic Syndrome/enzymology/metabolism
MH  - NF-kappa B/*metabolism
MH  - Protein Kinase C-delta/*metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Up-Regulation
EDAT- 2009/08/12 09:00
MHDA- 2010/03/05 06:00
CRDT- 2009/08/12 09:00
PHST- 2009/04/04 00:00 [received]
PHST- 2009/06/09 00:00 [revised]
PHST- 2009/07/06 00:00 [accepted]
PHST- 2009/08/12 09:00 [entrez]
PHST- 2009/08/12 09:00 [pubmed]
PHST- 2010/03/05 06:00 [medline]
AID - S1043-4666(09)00187-2 [pii]
AID - 10.1016/j.cyto.2009.07.008 [doi]
PST - ppublish
SO  - Cytokine. 2009 Dec;48(3):186-95. doi: 10.1016/j.cyto.2009.07.008. Epub 2009 Aug 
      6.