PMID- 24517399
OWN - NLM
STAT- MEDLINE
DCOM- 20140826
LR  - 20211021
IS  - 1475-2840 (Electronic)
IS  - 1475-2840 (Linking)
VI  - 13
DP  - 2014 Feb 12
TI  - Vaspin inhibits cytokine-induced nuclear factor-kappa B activation and adhesion 
      molecule expression via AMP-activated protein kinase activation in vascular 
      endothelial cells.
PG  - 41
LID - 10.1186/1475-2840-13-41 [doi]
AB  - BACKGROUND: Vaspin is an adipocytokine that was recently identified in the 
      visceral adipose tissue of diabetic rats and has anti-diabetic and 
      anti-atherogenic effects. We hypothesized that vaspin prevents inflammatory 
      cytokine-induced nuclear factor-kappa B (NF-kappaB) activation by activating 
      AMP-activated protein kinase (AMPK) in vascular endothelial cells. METHODS: We 
      examined the effects of vaspin on NF-kappaB activation and the expression of the 
      NF-kappaB-mediated genes intercellular adhesion molecule-1 (ICAM-1), vascular cell 
      adhesion molecule-1 (VCAM-1), E-selectin, and monocyte chemoattractant protein-1 
      (MCP-1). Human aortic endothelial cells (HAECS) were used. Tumor necrosis factor 
      alpha (TNFalpha) was used as a representative proinflammatory cytokine. RESULTS: 
      Treatment with vaspin significantly increased the phosphorylation of AMPK and 
      acetyl-CoA carboxylase, the down-stream target of AMPK. Furthermore, treatment 
      with vaspin significantly decreased TNFalpha-induced activation of NF-kappaB, as well as 
      the expression of the adhesion molecules ICAM-1, VCAM-1, E-selectin, and MCP-1. 
      These effects were abolished following transfection of AMPKalpha1-specific small 
      interfering RNA. In an adhesion assay using THP-1 cells, vaspin reduced 
      TNFalpha-induced adhesion of monocytes to HAECS in an AMPK-dependent manner. 
      CONCLUSIONS: Vaspin might attenuate the cytokine-induced expression of adhesion 
      molecule genes by inhibiting NF-kappaB following AMPK activation.
FAU - Jung, Chang Hee
AU  - Jung CH
FAU - Lee, Min Jung
AU  - Lee MJ
FAU - Kang, Yu Mi
AU  - Kang YM
FAU - Lee, Yoo La
AU  - Lee YL
FAU - Yoon, Hae Kyeong
AU  - Yoon HK
FAU - Kang, Sang-Wook
AU  - Kang SW
FAU - Lee, Woo Je
AU  - Lee WJ
FAU - Park, Joong-Yeol
AU  - Park JY
AD  - Department of Internal Medicine, University of Ulsan College of Medicine, 
      Poongnap-dong, Songpa-gu, Seoul 138-736, Korea. jypark@amc.seoul.kr.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20140212
PL  - England
TA  - Cardiovasc Diabetol
JT  - Cardiovascular diabetology
JID - 101147637
RN  - 0 (Cell Adhesion Molecules)
RN  - 0 (Cytokines)
RN  - 0 (NF-kappa B)
RN  - 0 (SERPINA12 protein, human)
RN  - 0 (Serpins)
RN  - EC 2.7.11.31 (AMP-Activated Protein Kinases)
SB  - IM
MH  - AMP-Activated Protein Kinases/*metabolism
MH  - Cell Adhesion Molecules/antagonists & inhibitors/*biosynthesis
MH  - Cells, Cultured
MH  - Cytokines/antagonists & inhibitors/*pharmacology
MH  - Endothelial Cells/drug effects/*metabolism
MH  - Humans
MH  - NF-kappa B/antagonists & inhibitors/*metabolism
MH  - Serpins/*pharmacology
PMC - PMC3925442
EDAT- 2014/02/13 06:00
MHDA- 2014/08/27 06:00
PMCR- 2014/02/12
CRDT- 2014/02/13 06:00
PHST- 2013/11/20 00:00 [received]
PHST- 2014/02/11 00:00 [accepted]
PHST- 2014/02/13 06:00 [entrez]
PHST- 2014/02/13 06:00 [pubmed]
PHST- 2014/08/27 06:00 [medline]
PHST- 2014/02/12 00:00 [pmc-release]
AID - 1475-2840-13-41 [pii]
AID - 10.1186/1475-2840-13-41 [doi]
PST - epublish
SO  - Cardiovasc Diabetol. 2014 Feb 12;13:41. doi: 10.1186/1475-2840-13-41.