PMID- 19166999
OWN - NLM
STAT- MEDLINE
DCOM- 20090825
LR  - 20161125
IS  - 1879-1484 (Electronic)
IS  - 0021-9150 (Linking)
VI  - 205
IP  - 1
DP  - 2009 Jul
TI  - Pre-B cell colony enhancing factor (PBEF)/visfatin induces secretion of MCP-1 in 
      human endothelial cells: role in visfatin-induced angiogenesis.
PG  - 113-9
LID - 10.1016/j.atherosclerosis.2008.11.024 [doi]
AB  - OBJECTIVES: Visfatin and Monocyte-Chemoattractant-Protein-1 (MCP-1) are elevated 
      in cardiovascular pathologies, insulin-resistant and diabetic states. Visfatin 
      has been reported to exhibit pro-angiogenic actions in human endothelial cells. 
      Given MCP-1's well described pro-angiogenic properties we sought to study the 
      potential interaction between visfatin and MCP-1 in human endothelial cells. We 
      also explored the possible autocrine/paracrine mechanisms governing this 
      potential interaction; specifically we looked at the effect of visfatin on 
      MCP-1's putative receptor (CCR2 receptor) in human endothelial cells. METHODS AND 
      RESULTS: Using in vitro angiogenic assays (capillary tube formation and 
      migration), Western blotting and RT-PCR, we found that visfatin, 
      dose-dependently, induced MCP-1 as well as CCR2 levels. We also studied the 
      involvement of PI3Kinase, MAPKinase and NF-kappaB pathways in visfatin induced 
      MCP-1/CCR2 levels by employing LY294002, U0126 and BAY11-7085, respectively. We 
      found the increase in MCP-1 and CCR2 levels by visfatin were negated by LY294002 
      and BAY11-7085, but not with U0126, suggesting the crucial role of PI3Kinase and 
      NF-kappaB pathways in visfatin induced MCP-1 and its autocrine regulation via the 
      CCR2 receptor. Finally, we consolidate the role of MCP-1 in visfatin-induced 
      angiogenesis by employing CCR2 antagonist (RS-102895) and MCP-1 neutralising 
      antibody, respectively. CONCLUSIONS: Our novel data reveal that MCP-1 is pivotal 
      in modulating visfatin-induced angiogenesis via NF-kappaB and PI3Kinase pathways. 
      Furthermore, our findings elucidate the potential influence of 
      autocrine/paracrine mechanisms (via the CCR2 receptor) underlying visfatin's 
      angiogenic effects through MCP-1.
FAU - Adya, Raghu
AU  - Adya R
AD  - Endocrinology & Metabolism Group, Clinical Sciences Research Institute, Warwick 
      Medical School, University of Warwick, Coventry, UK.
FAU - Tan, Bee K
AU  - Tan BK
FAU - Chen, Jing
AU  - Chen J
FAU - Randeva, Harpal S
AU  - Randeva HS
LA  - eng
PT  - Journal Article
DEP - 20081203
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (BAY 11-7085)
RN  - 0 (Butadienes)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chromones)
RN  - 0 (Cytokines)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Morpholines)
RN  - 0 (NF-kappa B)
RN  - 0 (Nitriles)
RN  - 0 (Sulfones)
RN  - 0 (U 0126)
RN  - 31M2U1DVID (2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one)
RN  - EC 2.4.2.12 (Nicotinamide Phosphoribosyltransferase)
RN  - EC 2.4.2.12 (nicotinamide phosphoribosyltransferase, human)
RN  - EC 2.7.1.- (Phosphatidylinositol 3-Kinases)
SB  - IM
MH  - Butadienes/pharmacology
MH  - Cell Movement
MH  - Chemokine CCL2/*metabolism
MH  - Chromones/pharmacology
MH  - Cytokines/*metabolism
MH  - Endothelial Cells/metabolism
MH  - Enzyme Inhibitors/pharmacology
MH  - Humans
MH  - Models, Biological
MH  - Morpholines/pharmacology
MH  - NF-kappa B/metabolism
MH  - Neovascularization, Pathologic
MH  - Nicotinamide Phosphoribosyltransferase/*metabolism
MH  - Nitriles/pharmacology
MH  - Phosphatidylinositol 3-Kinases/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Sulfones/pharmacology
EDAT- 2009/01/27 09:00
MHDA- 2009/08/26 09:00
CRDT- 2009/01/27 09:00
PHST- 2008/08/08 00:00 [received]
PHST- 2008/11/11 00:00 [revised]
PHST- 2008/11/19 00:00 [accepted]
PHST- 2009/01/27 09:00 [entrez]
PHST- 2009/01/27 09:00 [pubmed]
PHST- 2009/08/26 09:00 [medline]
AID - S0021-9150(08)00820-4 [pii]
AID - 10.1016/j.atherosclerosis.2008.11.024 [doi]
PST - ppublish
SO  - Atherosclerosis. 2009 Jul;205(1):113-9. doi: 
      10.1016/j.atherosclerosis.2008.11.024. Epub 2008 Dec 3.