PMID- 16795034
OWN - NLM
STAT- MEDLINE
DCOM- 20061213
LR  - 20161124
IS  - 0730-2312 (Print)
IS  - 0730-2312 (Linking)
VI  - 99
IP  - 4
DP  - 2006 Nov 1
TI  - Lysophospholipids increase IL-8 and MCP-1 expressions in human umbilical cord 
      vein endothelial cells through an IL-1-dependent mechanism.
PG  - 1216-32
AB  - Lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S1P) are both 
      low-molecular-weight lysophospholipid (LPL) ligands which are recognized by the 
      Edg family of G protein-coupled receptors (GPCRs). In endothelial cells, these 
      two ligands activate Edg receptors resulting in cell proliferation and cell 
      migration. Interleukin-8 (IL-8) is a C-X-C chemokine and acts as a 
      chemoattractant of neutrophils, whereas monocyte chemoattractant protein-1 
      (MCP-1) is a C-C chemokine and functions mainly as a chemoattractant of 
      monocytes/macrophages. Both factors are secreted from endothelial cells and have 
      been implicated in the processes leading to atherosclerosis. We examined the 
      effects of LPLs on the expression of IL-8 and MCP-1, key regulators of leukocyte 
      recruitment in human umbilical cord vein endothelial cells (HUVECs). Work 
      illustrated in this article showed that LPA and S1P enhanced IL-8 and MCP-1 mRNA 
      expressions, and protein secretions in dose- and time-dependent fashions. Maximal 
      mRNA expression appeared at 16 hr post-ligand treatment. Using prior treatments 
      with chemical inhibitors, LPLs enhanced IL-8 and MCP-1 expressions through a Gi-, 
      Rho-, and NFkappaB-dependent mechanism. In a chemotaxis assay system, LPL 
      treatments of endothelial cells enhanced monocyte recruitment through 
      upregulating IL-8 and MCP-1 protein secretions. Pre-incubation with AF12198, an 
      IL-1 receptor antagonist or IL-1 functional blocking antibody both suppressed the 
      enhanced effects elicited by LPLs of IL-8 and MCP-1 mRNA expressions in HUVECs. 
      These results suggest that LPLs released by activated platelets might enhance the 
      IL-8- and MCP-1-dependent chemoattraction of monocytes toward the endothelium 
      through an IL-1-dependent mechanism, which may play an important role in 
      facilitating wound-healing and inflammation processes.
FAU - Lin, Chi Iou
AU  - Lin CI
AD  - Institute of Zoology, National Taiwan University, Taipei, Taiwan.
FAU - Chen, Chiung-Nien
AU  - Chen CN
FAU - Chen, Jiun Hong
AU  - Chen JH
FAU - Lee, Hsinyu
AU  - Lee H
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - J Cell Biochem
JT  - Journal of cellular biochemistry
JID - 8205768
RN  - 0 (Carrier Proteins)
RN  - 0 (Chemokine CCL2)
RN  - 0 (EXOC3 protein, human)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-8)
RN  - 0 (Lysophospholipids)
RN  - 0 (RNA, Messenger)
RN  - 0 (Thiocarbamates)
RN  - 0 (Vesicular Transport Proteins)
RN  - 135467-92-4 (prolinedithiocarbamate)
RN  - 26993-30-6 (sphingosine 1-phosphate)
RN  - 9DLQ4CIU6V (Proline)
RN  - EC 2.4.2.31 (Pertussis Toxin)
RN  - NGZ37HRE42 (Sphingosine)
RN  - PG6M3969SG (lysophosphatidic acid)
SB  - IM
MH  - Carrier Proteins/pharmacology
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Chemotaxis/drug effects
MH  - Endothelial Cells/*cytology/*drug effects
MH  - Humans
MH  - Interleukin-1/*metabolism
MH  - Interleukin-8/genetics/*metabolism
MH  - Lysophospholipids/*pharmacology
MH  - Pertussis Toxin/pharmacology
MH  - Proline/analogs & derivatives/pharmacology
MH  - RNA, Messenger/genetics/metabolism
MH  - Sphingosine/analogs & derivatives/pharmacology
MH  - Thiocarbamates/pharmacology
MH  - Time Factors
MH  - Umbilical Veins/*cytology/drug effects
MH  - Up-Regulation/drug effects
MH  - Vesicular Transport Proteins
EDAT- 2006/06/24 09:00
MHDA- 2006/12/14 09:00
CRDT- 2006/06/24 09:00
PHST- 2006/06/24 09:00 [pubmed]
PHST- 2006/12/14 09:00 [medline]
PHST- 2006/06/24 09:00 [entrez]
AID - 10.1002/jcb.20963 [doi]
PST - ppublish
SO  - J Cell Biochem. 2006 Nov 1;99(4):1216-32. doi: 10.1002/jcb.20963.