PMID- 18055523
OWN - NLM
STAT- MEDLINE
DCOM- 20080331
LR  - 20200930
IS  - 0363-6135 (Print)
IS  - 0363-6135 (Linking)
VI  - 294
IP  - 2
DP  - 2008 Feb
TI  - Cardiotrophin-1 stimulates intercellular adhesion molecule-1 and monocyte 
      chemoattractant protein-1 in human aortic endothelial cells.
PG  - H750-63
AB  - Intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 
      (MCP-1) play critical roles in mediating monocyte adhesion to the vascular 
      endothelium and monocyte migration into the subendothelial regions of the 
      vessels. Inasmuch as cardiotrophin-1 (CT-1), an IL-6-type cytokine, was expressed 
      in human atherosclerotic plaque, we examined whether CT-1 induces monocyte 
      adhesion and migration by stimulating gene and protein expressions of ICAM-1 and 
      MCP-1 in human aortic endothelial cells (HAECs). Immunocytochemistry revealed 
      that CT-1 increased intensity of ICAM-1 and MCP-1 immunoreactivity in HAECs. 
      Adhesion assay and chemotaxis assay revealed that CT-1 increased human monocytic 
      THP-1 cell adhesion to HAECs and promoted chemotaxis in THP-1 cells, which were 
      attenuated by anti-ICAM-1 and anti-MCP-1 antibody, respectively. Western blot 
      analysis showed that CT-1 increased phosphorylation of ERK1/2 MAP kinase, p38 MAP 
      kinase, and Akt and that their inhibitors, PD-98059, SB-203580, and LY-294002, 
      respectively, inhibited phosphorylation. RNase protection assay and ELISA 
      demonstrated that CT-1 increased gene and protein expressions of ICAM-1 and 
      MCP-1. EMSA revealed that CT-1 enhanced NF-kappaB DNA-binding activity. 
      CT-1-mediated upregulation of ICAM-1 and MCP-1 was suppressed by PD-98059, 
      SB-203580, LY-294002, and parthenolide. The present study demonstrates that CT-1 
      promotes monocyte adhesion and migration by stimulating ICAM-1 and MCP-1 through 
      mechanisms that involve ERK1/2 MAP kinase, p38 MAP kinase, phosphatidylinositol 
      3-kinase, and NF-kappaB pathways and suggests that CT-1 plays an important role 
      in the pathophysiology of vascular inflammation and atherosclerosis.
FAU - Ichiki, Tomoko
AU  - Ichiki T
AD  - Institute for Clinical Research, National Hospital Organization Kagoshima Medical 
      Center, 8-1 Shiroyama-cho, Kagoshima 892-0853, Japan.
FAU - Jougasaki, Michihisa
AU  - Jougasaki M
FAU - Setoguchi, Manabu
AU  - Setoguchi M
FAU - Imamura, Junichi
AU  - Imamura J
FAU - Nakashima, Hitoshi
AU  - Nakashima H
FAU - Matsuoka, Tatsuru
AU  - Matsuoka T
FAU - Sonoda, Masahiro
AU  - Sonoda M
FAU - Nakamura, Kazuhiko
AU  - Nakamura K
FAU - Minagoe, Shinichi
AU  - Minagoe S
FAU - Tei, Chuwa
AU  - Tei C
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20071130
PL  - United States
TA  - Am J Physiol Heart Circ Physiol
JT  - American journal of physiology. Heart and circulatory physiology
JID - 100901228
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Indicators and Reagents)
RN  - 0 (LIFR protein, human)
RN  - 0 (Leukemia Inhibitory Factor Receptor alpha Subunit)
RN  - 0 (NF-kappa B)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 133483-10-0 (Cytokine Receptor gp130)
RN  - 63231-63-0 (RNA)
RN  - AJ7U77BR8I (cardiotrophin 1)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Aged
MH  - Atherosclerosis/pathology
MH  - Blotting, Western
MH  - Cell Adhesion/drug effects
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis
MH  - Chemotaxis/drug effects
MH  - Cytokine Receptor gp130/biosynthesis
MH  - Cytokines/*pharmacology
MH  - Endothelial Cells/drug effects/*metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Female
MH  - Gene Expression/drug effects
MH  - Humans
MH  - Immunohistochemistry
MH  - Indicators and Reagents
MH  - Intercellular Adhesion Molecule-1/*biosynthesis
MH  - Leukemia Inhibitory Factor Receptor alpha Subunit/biosynthesis
MH  - Male
MH  - Mitogen-Activated Protein Kinases/antagonists & inhibitors/metabolism
MH  - NF-kappa B/metabolism
MH  - Nuclease Protection Assays
MH  - Phosphorylation
MH  - RNA/biosynthesis/isolation & purification
EDAT- 2007/12/07 09:00
MHDA- 2008/04/01 09:00
CRDT- 2007/12/07 09:00
PHST- 2007/12/07 09:00 [pubmed]
PHST- 2008/04/01 09:00 [medline]
PHST- 2007/12/07 09:00 [entrez]
AID - 00161.2007 [pii]
AID - 10.1152/ajpheart.00161.2007 [doi]
PST - ppublish
SO  - Am J Physiol Heart Circ Physiol. 2008 Feb;294(2):H750-63. doi: 
      10.1152/ajpheart.00161.2007. Epub 2007 Nov 30.