Abstract
The molecular mechanism of atherosclerosis is based on decreased expression of signal molecules connexin (Cx37 and Cx40), vascular endothelial growth factor (VEGF), and proliferative protein Ki-67, which characterize the processes of cell-cell interactions and proliferation of vascular endotheliocytes. Lys-Glu-Trp peptide in doses of 4 and 40 μg/ml promoted recovery of Cx37, Cx40, and VEGF expression in cultured endotheliocytes from the aorta of patients with atherosclerosis, which attests to vasoprotective effects of this agent.
MeSH terms
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Atherosclerosis / pathology*
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Cell Communication / drug effects*
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Cell Proliferation / drug effects*
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Cells, Cultured
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Connexins / metabolism
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Endothelial Cells / drug effects
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Endothelial Cells / physiology*
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Endothelium, Vascular / pathology
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Gap Junction alpha-4 Protein
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Gap Junction alpha-5 Protein
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Humans
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Ki-67 Antigen / metabolism
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Oligopeptides / pharmacology*
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Vascular Endothelial Growth Factor A / metabolism
Substances
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Connexins
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Ki-67 Antigen
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Oligopeptides
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VEGFA protein, human
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Vascular Endothelial Growth Factor A
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lysyl-glutamyl-tryptophan