PMID- 10559516
OWN - NLM
STAT- MEDLINE
DCOM- 20000106
LR  - 20190718
IS  - 0021-9150 (Print)
IS  - 0021-9150 (Linking)
VI  - 147
IP  - 2
DP  - 1999 Dec
TI  - Effect of vitamin E on human aortic endothelial cell production of chemokines and 
      adhesion to monocytes.
PG  - 297-307
AB  - Epidemiological and clinical studies indicate that vitamin E may reduce the risk 
      of cardiovascular disease (CVD). Modulation of adhesion molecule expression and 
      chemokine production by vitamin E may contribute to its beneficial effect. In 
      this study we found that the enrichment of confluent human aortic endothelial 
      cells (HAEC) or U937 monocytic cells with increasing doses of vitamin E 
      (d-alpha-tocopherol, 20, 40, and 60 micromol/l for 20 h) inhibited their adhesion 
      when either or both cell types were stimulated with interleukin (IL)-1beta. 
      Enrichment of HAEC with the same doses of vitamin E suppressed 
      IL-1beta-stimulated expression of intercellular adhesion molecule-1 (ICAM-1), 
      vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion 
      molecule-1 (E-selectin). Supplementation with increasing doses of vitamin E up to 
      60 micromol/l was not effective in preventing spontaneous production of monocyte 
      chemoattractant protein-1 (MCP-1), but supplementation with vitamin E at 60 
      micromol/l reduced IL-8 production significantly. However, IL-1beta-induced 
      productions of both MCP-1 and IL-8 were dose-dependently suppressed by enrichment 
      of cells with vitamin E. Vitamin E, at the doses used, did not significantly 
      change the spontaneous production but dose-dependently inhibited the 
      IL-1beta-induced production of inflammatory cytokine IL-6. We concluded that 
      vitamin E could inhibit production of chemokines and inflammatory cytokines, in 
      addition to inhibiting adhesion of HAEC to monocytes by reducing expression of 
      adhesion molecules when cells were activated with an inflammatory cytokine. These 
      mediators are actively involved in the pathogenesis of atherosclerosis. 
      Therefore, their inhibition by vitamin E may contribute to vitamin E's reported 
      reduction in risk of CVD.
FAU - Wu, D
AU  - Wu D
AD  - Vascular Biology Laboratory and Nutritional Immunology Laboratory, JM USDA Human 
      Nutrition Research Center on Aging at Tufts University, Boston, MA 02111, USA.
FAU - Koga, T
AU  - Koga T
FAU - Martin, K R
AU  - Martin KR
FAU - Meydani, M
AU  - Meydani M
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - Ireland
TA  - Atherosclerosis
JT  - Atherosclerosis
JID - 0242543
RN  - 0 (E-Selectin)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Vascular Cell Adhesion Molecule-1)
RN  - 126547-89-5 (Intercellular Adhesion Molecule-1)
RN  - 1406-18-4 (Vitamin E)
SB  - IM
MH  - Analysis of Variance
MH  - Aorta
MH  - Cell Adhesion/*drug effects
MH  - Cells, Cultured
MH  - Dose-Response Relationship, Drug
MH  - E-Selectin/biosynthesis/drug effects
MH  - Endothelium, Vascular/cytology/*drug effects
MH  - Humans
MH  - Intercellular Adhesion Molecule-1/*drug effects/physiology
MH  - Interleukin-6/biosynthesis
MH  - Interleukin-8/biosynthesis
MH  - Monocytes/drug effects/*metabolism
MH  - Sensitivity and Specificity
MH  - Vascular Cell Adhesion Molecule-1/*drug effects/physiology
MH  - Vitamin E/pharmacokinetics/*pharmacology
EDAT- 1999/11/24 00:00
MHDA- 1999/11/24 00:01
CRDT- 1999/11/24 00:00
PHST- 1999/11/24 00:00 [pubmed]
PHST- 1999/11/24 00:01 [medline]
PHST- 1999/11/24 00:00 [entrez]
AID - S0021-9150(99)00199-9 [pii]
AID - 10.1016/s0021-9150(99)00199-9 [doi]
PST - ppublish
SO  - Atherosclerosis. 1999 Dec;147(2):297-307. doi: 10.1016/s0021-9150(99)00199-9.