PMID- 18949387
OWN - NLM
STAT- MEDLINE
DCOM- 20090203
LR  - 20221207
IS  - 1107-3756 (Print)
IS  - 1107-3756 (Linking)
VI  - 22
IP  - 5
DP  - 2008 Nov
TI  - Glucosamine, a naturally occurring amino monosaccharide modulates LL-37-induced 
      endothelial cell activation.
PG  - 657-62
AB  - Atheroscleros is now considered as a chronic inflammatory disease, and 
      glucosamine has a potential to exhibit anti-inflammatory action. Thus, we 
      investigated the effect of glucosamine on LL-37-induced endothelial cell 
      activation. HUVEC (human umbilical vein endothelial cells) were stimulated by 
      LL-37 in the presence or absence of glucosamine (0.01-1 mM) or its analogue, 
      N-acetylglucosamine (0.1-1 mM). mRNA expression of MCP-1 (monocyte 
      chemoattractant protein-1) and ICAM-1 (intercellular adhesion molecule-1) was 
      evaluated by real-time RT-PCR, and their protein levels were analyzed by ELISA 
      and Western blotting, respectively. Furthermore, the effect of glucosamine on 
      O-N-acetylglucosamine (O-GlcNAc) modification was evaluated by Western blotting. 
      Glucosamine but not N-acetylglucosamine suppressed the LL-37-induced expression 
      of MCP-1 and ICAM-1 at both mRNA (p<0.05 at 0.1 mM) and protein levels (p<0.05 at 
      1 mM). Of interest, O-GlcNAc modification was induced by incubating HUVEC with 
      glucosamine (p<0.05 at 1 mM) but not N-acetylglucosamine. Of note, alloxan, an 
      O-N-acetylglucosamine transferase inhibitor, which prevented the 
      glucosamine-induced O-GlcNAc modification, abrogated the suppressive effect of 
      glucosamine on MCP-1 and ICAM-1 expression (p<0.05 at 0.5 mM). These observations 
      suggest that glucosamine modulates endothelial cell activation possibly via 
      O-GlcNAc modification, and may exhibit an anti-inflammatory action on 
      atherosclerosis.
FAU - Ju, Yinghua
AU  - Ju Y
AD  - Department of Host Defense and Biochemical Research, Juntendo University, School 
      of Medicine, Hongo, 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 (Antimicrobial Cationic Peptides)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - V956696549 (Acetylglucosamine)
RN  - 0 (Cathelicidins)
SB  - IM
MH  - Acetylglucosamine/*metabolism
MH  - Antimicrobial Cationic Peptides/*pharmacology
MH  - Atherosclerosis/*metabolism/pathology
MH  - Cells, Cultured
MH  - Chemokine CCL2/biosynthesis
MH  - Endothelial Cells/*metabolism/pathology
MH  - Gene Expression Regulation/drug effects
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/biosynthesis
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Umbilical Veins/*metabolism/pathology
MH  - Cathelicidins
EDAT- 2008/10/25 09:00
MHDA- 2009/02/04 09:00
CRDT- 2008/10/25 09:00
PHST- 2008/10/25 09:00 [pubmed]
PHST- 2009/02/04 09:00 [medline]
PHST- 2008/10/25 09:00 [entrez]
PST - ppublish
SO  - Int J Mol Med. 2008 Nov;22(5):657-62.