PMID- 19020780
OWN - NLM
STAT- MEDLINE
DCOM- 20090716
LR  - 20131121
IS  - 1107-3756 (Print)
IS  - 1107-3756 (Linking)
VI  - 22
IP  - 6
DP  - 2008 Dec
TI  - Modulation of TNF-alpha-induced endothelial cell activation by glucosamine, a 
      naturally occurring amino monosaccharide.
PG  - 809-15
AB  - Atherosclerosis is now considered a chronic inflammatory disease, and glucosamine 
      has the potential to exhibit an anti-inflammatory action. Thus, we investigated 
      the effect of glucosamine on tumor necrosis factor alpha (TNF-alpha)-induced 
      endothelial cell activation. Human umbilical vein endothelial cells (HUVECs) were 
      stimulated by TNF-alpha in the presence or absence of glucosamine or its 
      analogue, N-acetylglucosamine. mRNA expression of MCP-1 (a chemoattractant 
      protein) and ICAM-1 (an adhesion molecule) was evaluated by real-time RT-PCR, and 
      their protein levels were analyzed by ELISA and Western blotting, respectively. 
      Furthermore, the effects of glucosamine on the phosphorylation of p38MAPK and 
      NF-kappaB, and O-N-acetylglucosamine (O-GlcNAc) modification were evaluated by 
      Western blotting. The results demonstrated that glucosamine but not 
      N-acetylglucosamine suppressed TNF-alpha-induced expression of MCP-1 and ICAM-1 
      at both the mRNA and protein levels. Furthermore, glucosamine abrogated the 
      phosphorylation of p38MAPK and NF-kappaB. To note, glucosamine induced O-GlcNAc 
      modification, which was negatively correlated with the expression of MCP-1 and 
      ICAM-1, and phosphorylation of p38MAPK and NF-kappaB. Thus, glucosamine is likely 
      to suppress endothelial cell activation (TNF-alpha-induced ICAM-1 and MCP-1 
      expression) possibly by affecting p38MAPK and NF-kappaB signaling via O-GlcNAc 
      modification.
FAU - Ju, Yinghua
AU  - Ju Y
AD  - Department of Host Defense and Biochemical Research, Juntendo University, School 
      of Medicine, Hongo, Bunkyo-ku, Tokyo 113-8421, Japan.
FAU - Hua, Jian
AU  - Hua J
FAU - Sakamoto, Koji
AU  - Sakamoto K
FAU - Ogawa, Hideoki
AU  - Ogawa H
FAU - Nagaoka, Isao
AU  - Nagaoka I
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Greece
TA  - Int J Mol Med
JT  - International journal of molecular medicine
JID - 9810955
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - EC 2.7.11.24 (p38 Mitogen-Activated Protein Kinases)
RN  - N08U5BOQ1K (Glucosamine)
SB  - IM
MH  - Chemokine CCL2/metabolism
MH  - Endothelial Cells/drug effects/*metabolism
MH  - Glucosamine/analogs & derivatives/*pharmacology
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/metabolism
MH  - NF-kappa B/metabolism
MH  - Signal Transduction/drug effects
MH  - Tumor Necrosis Factor-alpha/*metabolism
MH  - Umbilical Veins/cytology
MH  - p38 Mitogen-Activated Protein Kinases/metabolism
EDAT- 2008/11/21 09:00
MHDA- 2009/07/17 09:00
CRDT- 2008/11/21 09:00
PHST- 2008/11/21 09:00 [pubmed]
PHST- 2009/07/17 09:00 [medline]
PHST- 2008/11/21 09:00 [entrez]
PST - ppublish
SO  - Int J Mol Med. 2008 Dec;22(6):809-15.