Inhibition of macrophage-mediated low density lipoprotein oxidation by stimulated rat serosal mast cells

Mast cells and macrophages coexist in the human arterial intima where oxidation of low density lipoproteins (LDL) also takes place during atherosclerosis. To investigate whether mast cells play a role in macrophage-mediated oxidation of LDL, a model system was designed in which mast cells and macrop...

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Published inThe Journal of biological chemistry Vol. 268; no. 11; pp. 7741 - 7746
Main Author LINDSTEDT, K. A
Format Journal Article
LanguageEnglish
Published Bethesda, MD American Society for Biochemistry and Molecular Biology 15.04.1993
Subjects
Analytical, structural and metabolic biochemistry
Animals
Biological and medical sciences
Cell Communication
Cells, Cultured
Copper - pharmacology
Copper Sulfate
Cytoplasmic Granules - metabolism
Egtazic Acid - pharmacology
Exocytosis
Fundamental and applied biological sciences. Psychology
Histamine - pharmacology
Humans
Kinetics
Lipoproteins, LDL - metabolism
Lipoproteins, myelin
Macrophages - drug effects
Macrophages - metabolism
Mast Cells - physiology
Mice
Oxidation-Reduction
p-Methoxy-N-methylphenethylamine - pharmacology
Proteins
Proteoglycans - pharmacology
Rats
Thiobarbituric Acid Reactive Substances - analysis
Lipoprotein LDL
Histamine
Vertebrata
Mammalia
Rat
Rodentia
Atherosclerosis
Mast cell
Oxidation
Inhibition
Macrophage
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Abstract Mast cells and macrophages coexist in the human arterial intima where oxidation of low density lipoproteins (LDL) also takes place during atherosclerosis. To investigate whether mast cells play a role in macrophage-mediated oxidation of LDL, a model system was designed in which mast cells and macrophages were cocultured in incubation medium containing LDL. Stimulation of rat serosal mast cells to induce exocytosis of their cytoplasmic granules was found to inhibit macrophage-mediated oxidation of LDL. The inhibitory effect depended on the ability of mast cell-derived histamine, released from the exocytosed granules into the medium, to bind the copper ions necessary for propagation of the macrophage-initiated oxidation of LDL. In addition to binding free copper ions, the mast cell-derived histamine was also capable of inhibiting oxidation of LDL propagated by copper ions bound to the apolipoprotein B component of the LDL particle. The results indicate that mast cells may prevent cell-mediated oxidation of LDL and imply a potentially preventive role for the mast cell in atherosclerosis.
AbstractList Mast cells and macrophages coexist in the human arterial intima where oxidation of low density lipoproteins (LDL) also takes place during atherosclerosis. To investigate whether mast cells play a role in macrophage-mediated oxidation of LDL, a model system was designed in which mast cells and macrophages were cocultured in incubation medium containing LDL. Stimulation of rat serosal mast cells to induce exocytosis of their cytoplasmic granules was found to inhibit macrophage-mediated oxidation of LDL. The inhibitory effect depended on the ability of mast cell-derived histamine, released from the exocytosed granules into the medium, to bind the copper ions necessary for propagation of the macrophage-initiated oxidation of LDL. In addition to binding free copper ions, the mast cell-derived histamine was also capable of inhibiting oxidation of LDL propagated by copper ions bound to the apolipoprotein B component of the LDL particle. The results indicate that mast cells may prevent cell-mediated oxidation of LDL and imply a potentially preventive role for the mast cell in atherosclerosis.
Mast cells and macrophages coexist in the human arterial intima where oxidation of low density lipoproteins (LDL) also takes place during atherosclerosis. To investigate whether mast cells play a role in macrophage-mediated oxidation of LDL, a model system was designed in which mast cells and macrophages were cocultured in incubation medium containing LDL. Stimulation of rat serosal mast cells to induce exocytosis of their cytoplasmic granules was found to inhibit macrophage-mediated oxidation of LDL. The inhibitory effect depended on the ability of mast cell-derived histamine, released from the exocytosed granules into the medium, to bind the copper ions necessary for propagation of the macrophage-initiated oxidation of LDL. In addition to binding free copper ions, the mast cell-derived histamine was also capable of inhibiting oxidation of LDL propagated by copper ions bound to the apolipoprotein B component of the LDL particle. The results indicate that mast cells may prevent cell-mediated oxidation of LDL and imply a potentially preventive role for the mast cell in atherosclerosis.
Author K A Lindstedt
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Issue 11
Keywords Lipoprotein LDL
Histamine
Vertebrata
Mammalia
Rat
Rodentia
Atherosclerosis
Mast cell
Oxidation
Inhibition
Macrophage
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Snippet Mast cells and macrophages coexist in the human arterial intima where oxidation of low density lipoproteins (LDL) also takes place during atherosclerosis. To...
Mast cells and macrophages coexist in the human arterial intima where oxidation of low density lipoproteins (LDL) also takes place during atherosclerosis. To...
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SubjectTerms Analytical, structural and metabolic biochemistry
Animals
Biological and medical sciences
Cell Communication
Cells, Cultured
Copper - pharmacology
Copper Sulfate
Cytoplasmic Granules - metabolism
Egtazic Acid - pharmacology
Exocytosis
Fundamental and applied biological sciences. Psychology
Histamine - pharmacology
Humans
Kinetics
Lipoproteins, LDL - metabolism
Lipoproteins, myelin
Macrophages - drug effects
Macrophages - metabolism
Mast Cells - physiology
Mice
Oxidation-Reduction
p-Methoxy-N-methylphenethylamine - pharmacology
Proteins
Proteoglycans - pharmacology
Rats
Thiobarbituric Acid Reactive Substances - analysis
Title Inhibition of macrophage-mediated low density lipoprotein oxidation by stimulated rat serosal mast cells
URI http://www.jbc.org/content/268/11/7741.abstract
https://www.ncbi.nlm.nih.gov/pubmed/8463303
https://search.proquest.com/docview/75668045
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