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Cited by 19Antioxidant Activity and Oxidative StressNitric Oxide and Endothelin EffectsAtherosclerosis and Cardiovascular Diseases

Vitamin E Inhibits Lysophosphatidylcholine-Induced Endothelial Dysfunction and Platelet Activation

Murohara, Toyoaki, Ikeda, Hisao, Katoh, Atsushi, Takajo, Yoshinori, Otsuka, Yoritaka, Haramaki, Nobuya, Imaizumi, Tsutomu·2002·Antioxidants & Redox Signaling
DOI 10.1089/152308602760598945
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Abstract

Lysophosphatidylcholine (LPC), a lysolipid contained in oxidized low-density lipoprotein, is an atherogenic molecule that induces endothelial dysfunction and platelet activation and inhibits angiogenesis. Although studies showed that vitamin E has antiatherogenic properties, the effects of vitamin E on LPC-induced endothelial dysfunction and platelet activation are little known. We examined whether vitamin E has protecting actions against LPC-induced alterations of endothelial and platelet functions. Incubation of cultured bovine aortic endothelial cells (BAECs) with LPC (10 microM) significantly inhibited bradykinin (1 microM)-stimulated nitric oxide release, which was prevented by cotreatment with vitamin E (50, 100, and 500 microg/ml) in a concentration-dependent manner. In isolated human platelets, LPC stimulated P-selectin expression and induced leukocyte-platelet interaction, which functionally depends on P-selectin expressed on the platelet surface. Vitamin E treatment significantly prevented the LPC-induced platelet P-selectin expression and leukocyte-platelet interaction. As LPC-induced endothelial dysfunction and platelet activation have been shown to involve the protein kinase C (PKC)-dependent signal transduction pathway, we examined the effects of vitamin E on LPC-induced PKC activation in human platelets and BAECs. Vitamin E significantly inhibited LPC (10 microM)-stimulated PKC activation in a concentration-dependent manner. It is concluded that (a) Vitamin E prevented LPC-induced endothelial dysfunction and preserved endothelial nitric oxide release, (b) vitamin E inhibited LPC-induced platelet activation (P-selectin expression) and leukocyte-platelet interaction, and (c) these mechanisms appeared to be at least partly mediated by suppression of the PKC in endothelial cells and platelets. The present findings may provide new insights into antiatherogenic mechanisms of vitamin E.

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Authors
Murohara, T., Ikeda, H., Katoh, A., Takajo, Y., Otsuka, Y., Haramaki, N., & Imaizumi, T.
Affiliations
Kurume University (JP)
ORCID
Venue
Antioxidants & Redox Signaling
Publisher
SAGE Publications
Published
2002-10
Volume
4
Issue
5
Pages
791-798
ISSN
  • 1523-0864 (ISSN-L)
  • 1557-7716
DOI
10.1089/152308602760598945
OpenAlex
W2049083049
Cited by
19
References
48
Citations by year
2025: 1 · 2024: 1 · 2023: 1 · 2022: 1 · 2020: 1 · 2016: 1 · 2015: 1 · 2014: 2 · 2013: 1 · 2012: 1
FWCI
0.58
Type
journal article
Language
en
Open access
closed
Locations
  • Antioxidants and Redox Signaling (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Biochemistry › Antioxidant Activity and Oxidative Stress
  • Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
  • Life Sciences › Immunology and Microbiology › Immunology › Atherosclerosis and Cardiovascular Diseases
Keywords
vitamin E, lysophosphatidylcholine, endothelial dysfunction, platelet activation, P-selectin, platelet-leukocyte interaction, protein kinase C, nitric oxide release, oxidized LDL, atherosclerosis
MeSH terms
Animals, Blood Platelets, Cattle, Cells, Cultured, Endothelium, Vascular, Enzyme Activation, Humans, Lysophosphatidylcholines, Platelet Aggregation Inhibitors, Protein Kinase C, Vitamin E, Platelet Activation, P-Selectin

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