PMID- 17097661
OWN - NLM
STAT- MEDLINE
DCOM- 20071016
LR  - 20220409
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 193
IP  - 2
DP  - 2007 Aug
TI  - Short-term high glucose exposure induces monocyte-endothelial cells adhesion and 
      transmigration by increasing VCAM-1 and MCP-1 expression in human aortic 
      endothelial cells.
PG  - 328-34
AB  - Acute, short-term hyperglycemia is becoming recognized as an important risk 
      factor for several diseases. In the present study, using human aortic endothelial 
      cells (HAECs), we investigated whether short-term high glucose exposure, either 
      on the scale of hours, could enhance the monocyte adhesion and migration to the 
      subendothelium via increasing expression of adhesion molecules and release of 
      chemotactic factors. HAECs stimulated with 25mM d(+)glucose (HG) for not more 
      than 12h, exhibited rapid up-regulation of vascular cell adhesion molecule-1 
      (VCAM-1) and monocyte chemoattractant protein-1 (MCP-1) mRNA and protein. 
      Although intercellular adhesion molecule-1 (ICAM-1) is considered as a marker of 
      the activation of the atherogenic process, early up-regulation was not observed, 
      and VCAM-1 and MCP-1 protein enhance was sufficient to increase the adhesiveness 
      of human monocytes U-937 to HAECs and their transmigration into the 
      subendothelial space after 4h HG stimulation; both effects were prevented by 
      interfering with monoclonal antibodies against VCAM-1, CD11b, and MCP-1. An 
      increased intracellular oxidative stress, a translocation of NF-kappaB to the 
      nucleus and a prevention of adhesion and transmigration of U-937 by interfering 
      with NF-kappaB inhibitors was also observed after a short HG treatment. Taken 
      together, these results suggest that either acute hyperglycemic spikes could 
      exert an influence on the onset of diabetic complications and on the development 
      of the atherogenic profile on diabetic and non-diabetic subjects.
FAU - Piga, Rosaria
AU  - Piga R
AD  - Department of Inflammation and Immunology, Graduate School of Medical Science, 
      Kyoto Prefectural University of Medicine, Kamigyo-ku, Kyoto, Japan. 
      ros-pi02@koto.kpu-m.ac.jp
FAU - Naito, Yuji
AU  - Naito Y
FAU - Kokura, Satoshi
AU  - Kokura S
FAU - Handa, Osamu
AU  - Handa O
FAU - Yoshikawa, Toshikazu
AU  - Yoshikawa T
LA  - eng
PT  - Journal Article
DEP - 20061113
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (Blood Glucose)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (NF-kappa B)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
SB  - IM
MH  - Blood Glucose/*immunology
MH  - Cell Adhesion/immunology
MH  - Cells, Cultured
MH  - Chemokine CCL2/*biosynthesis
MH  - Chemotaxis, Leukocyte/immunology
MH  - Endothelial Cells/*immunology
MH  - Humans
MH  - Monocytes/*immunology
MH  - NF-kappa B/immunology
MH  - Reactive Oxygen Species/immunology
MH  - Time Factors
MH  - Vascular Cell Adhesion Molecule-1/*biosynthesis
EDAT- 2006/11/14 09:00
MHDA- 2007/10/17 09:00
CRDT- 2006/11/14 09:00
PHST- 2006/01/05 00:00 [received]
PHST- 2006/08/12 00:00 [revised]
PHST- 2006/09/19 00:00 [accepted]
PHST- 2006/11/14 09:00 [pubmed]
PHST- 2007/10/17 09:00 [medline]
PHST- 2006/11/14 09:00 [entrez]
AID - S0021-9150(06)00583-1 [pii]
AID - 10.1016/j.atherosclerosis.2006.09.016 [doi]
PST - ppublish
SO  - Atherosclerosis. 2007 Aug;193(2):328-34. doi: 
      10.1016/j.atherosclerosis.2006.09.016. Epub 2006 Nov 13.