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Acute stress induces cardiac mast cell activation and histamine release, effects that are increased in Apolipoprotein
Man Huang1, Xinzhu Pang, Richard Letourneau
1Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, 136 Harrison Avenue, Boston, MA 02111, USA.
Insights
Acute stress releases histamine from cardiac mast cells in mice. Apolipoprotein E knockout mice show higher baseline histamine, suggesting a role in atherosclerosis development.
Area of Science:
- Cardiovascular Research
- Immunology
- Stress Physiology
Background:
- Cardiac mast cells are activated in atherosclerosis.
- Psychological stress can trigger acute coronary syndrome.
- Histamine, released by mast cells, is a coronary constrictor.
Purpose of the Study:
- Investigate the effect of acute stress on cardiac mast cell activation.
- Quantify cardiac and serum histamine levels in normal and ApoE knockout mice.
- Determine the source of histamine release during stress.
Main Methods:
- Utilized 8-14 week-old ApoE knockout and C57BL/6J mice.
- Measured cardiac and serum histamine levels before and after 120 min restraint stress.
- Assessed cardiac mast cell activation via light and electron microscopy.
- Confirmed histamine source using W/W(v) mast cell deficient mice.
Main Results:
- Restraint stress significantly reduced cardiac histamine and increased serum histamine in C57BL mice.
- ApoE knockout mice exhibited higher basal cardiac and serum histamine levels.
- Mast cell deficiency (W/W(v) mice) abolished stress-induced histamine release.
- ApoE knockout mice had a 37% higher number of cardiac mast cells.
Conclusions:
- Acute stress triggers mast cell-derived histamine release in the heart.
- Elevated basal histamine and mast cell numbers in ApoE knockout mice suggest a role in atherosclerosis.
- Findings enhance understanding of stress-related cardiovascular pathology.
Objectives:
Cardiac mast cells have recently been found to be activated in atherosclerotic coronary arteries, but no mediator has so far been documented to be released from them, nor have they been investigated in Apolipoprotein (Apo) E knockout (k/o) mice that develop atherosclerosis. Psychological stress triggers acute coronary syndrome, while acute restraint stress stimulates rat cardiac mast cells, the main mediator of which histamine is a coronary constrictor. Here, we investigated the effect of acute stress on the activation of cardiac mast cells morphologically, as well as the levels of cardiac and serum histamine in normal and genetically deficient mice.
Methods:
Male, 8-14 week-old ApoE k/o mice and their corresponding control C57BL/6J mice were used. Significant reduction of cardiac histamine from 396.7+/-45.6 to 214.6+/-41.5 ng/g was observed over 120 min restraint stress with a corresponding increase in serum histamine from 126.9+/-4.0 to 188.4+/-17.3 ng/ml in C57BL mice. Cardiac mast cell activation was observed by light and electron microscopy. Both basal cardiac and serum histamine in ApoE k/o mice was significantly higher than that in C57BL mice. Although the extent of mast cell activation in ApoE k/o mice was similar to that of C57BL mice, the number of cardiac mast cells in ApoE k/o mice was 37% higher. Histamine levels were hardly detectable with or without stress in W/W(v) mast cell deficient mice.
Conclusions:
Acute restraint stress triggered cardiac histamine release in mice that was clearly derived from mast cells, as it was absent in W/W(v) mice. The high basal cardiac and serum histamine in ApoE k/o mice, along with the high number of cardiac mast cells, suggest possible ongoing cardiac mast cell activation that may participate in atherosclerosis. These results may possibly help better understand stress-related cardiovascular pathology.