PMID- 20551970
OWN - NLM
STAT- MEDLINE
DCOM- 20110203
LR  - 20211020
IS  - 1559-7016 (Electronic)
IS  - 0271-678X (Print)
IS  - 0271-678X (Linking)
VI  - 31
IP  - 1
DP  - 2011 Jan
TI  - Sphingosylphosphorylcholine is a proinflammatory mediator in cerebral arteries.
PG  - 212-21
LID - 10.1038/jcbfm.2010.79 [doi]
AB  - Inflammation has an important function in the development of cerebral vasospasm 
      after subarachnoid hemorrhage (SAH); however, the mediators of this inflammatory 
      response have not been clearly identified. In this study, we have investigated 
      the potential function of two sphingolipids, which occur naturally in plasma and 
      serum, sphingosylphosphorylcholine (SPC) and sphingosine 1-phosphate (S1P), to 
      act as proinflammatory mediators in cerebral artery vascular smooth muscle (VSM) 
      cells. In rat cerebral arteries, SPC but not S1P activated p38 mitogen-activated 
      protein kinase (MAPK). Using transcription factor arrays, two proinflammatory 
      transcription factors activated by SPC in cerebral arteries were 
      identified--nuclear factor-kappaB and CCAAT-enhancer-binding protein. Both these 
      transcription factors were activated by SPC in a p38MAPK-dependent manner. To 
      determine whether this contributed to vascular inflammation, an inflammatory 
      protein array was performed, which showed that SPC increased release of the 
      chemokine monocyte chemoattractant protein-1 (MCP-1) in cultured rat VSM cells. 
      This increase in MCP-1 expression was confirmed in cerebral arteries. The S1P did 
      not increase MCP-1 release. Taken together, our results suggest that SPC, but not 
      S1P, can act as a proinflammatory mediator in cerebral arteries. This may 
      contribute to inflammation observed after SAH and may be part of the initiating 
      event in vasospasm.
FAU - Wirrig, Christiane
AU  - Wirrig C
AD  - Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen, 
      UK.
FAU - Hunter, Irene
AU  - Hunter I
FAU - Mathieson, Fiona A
AU  - Mathieson FA
FAU - Nixon, Graeme F
AU  - Nixon GF
LA  - eng
GR  - British Heart Foundation/United Kingdom
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20100616
PL  - United States
TA  - J Cereb Blood Flow Metab
JT  - Journal of cerebral blood flow and metabolism : official journal of the 
      International Society of Cerebral Blood Flow and Metabolism
JID - 8112566
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Inflammation Mediators)
RN  - 0 (Lysophospholipids)
RN  - 0 (NF-kappa B)
RN  - 0 (Transcription Factors)
RN  - 10216-23-6 (sphingosine phosphorylcholine)
RN  - 107-73-3 (Phosphorylcholine)
RN  - 26993-30-6 (sphingosine 1-phosphate)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - NGZ37HRE42 (Sphingosine)
SB  - IM
MH  - Animals
MH  - Blood Platelets/metabolism
MH  - Blotting, Western
MH  - Cells, Cultured
MH  - Cerebral Arteries/*metabolism/pathology
MH  - Chemokine CCL2/biosynthesis
MH  - Electrophoretic Mobility Shift Assay
MH  - Enzyme Activation/physiology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fluorescent Antibody Technique
MH  - Inflammation/chemically induced/pathology
MH  - Inflammation Mediators/*physiology
MH  - Lysophospholipids/metabolism
MH  - Male
MH  - Muscle, Smooth, Vascular/pathology
MH  - NF-kappa B/metabolism
MH  - Phosphorylcholine/*analogs & derivatives/metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sphingosine/*analogs & derivatives/metabolism/physiology
MH  - Subarachnoid Hemorrhage/pathology
MH  - Transcription Factors/genetics
MH  - Up-Regulation
MH  - Vasospasm, Intracranial/pathology
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
PMC - PMC3049485
EDAT- 2010/06/17 06:00
MHDA- 2011/02/04 06:00
PMCR- 2012/01/01
CRDT- 2010/06/17 06:00
PHST- 2010/06/17 06:00 [entrez]
PHST- 2010/06/17 06:00 [pubmed]
PHST- 2011/02/04 06:00 [medline]
PHST- 2012/01/01 00:00 [pmc-release]
AID - jcbfm201079 [pii]
AID - 10.1038/jcbfm.2010.79 [doi]
PST - ppublish
SO  - J Cereb Blood Flow Metab. 2011 Jan;31(1):212-21. doi: 10.1038/jcbfm.2010.79. Epub 
      2010 Jun 16.