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首页> 外文期刊>American Journal of Physiology >Modulation of cardiac mast cell-mediated extracellular matrix degradation by estrogen.
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Modulation of cardiac mast cell-mediated extracellular matrix degradation by estrogen.

机译：雌激素对心脏肥大细胞介导的细胞外基质降解的调节。

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There are fundamental differences between males and females with regard to susceptibility to heart disease. Although numerous animal models of heart failure have demonstrated that premenopausal females are afforded cardioprotection and, therefore, fare better in the face of cardiac disease than their male counterparts, many questions as to how this occurs still exist. Recently, we showed that 1) increased mast cell density is associated with adverse ventricular remodeling and 2) chemically induced mast cell degranulation using compound 48/80 resulted in remarkable changes in matrix metalloproteinase (MMP) activity, cardiac collagen structure, and cardiac diastolic function in normal male rats. With the known gender differences in cardiac disease in mind, we sought to examine the effects of chemically induced cardiac mast cell degranulation in isolated, blood-perfused hearts of intact female rats, ovariectomized female rats, and ovariectomized female rats treated with 17beta-estradiol. In response to mast cell degranulation, no significant differences in cardiac function, MMP-2 activity, or collagen volume fraction were observed between intact female rats and ovariectomized female rats treated with estrogen. In the ovariectomized female group, a significant rightward shift in the left ventricular pressure-volume relation, accompanied by a marked 133% increase in active MMP-2 values over that in the intact female group, was noted after treatment with compound 48/80 (P < or = 0.05), along with a significant reduction in collagen volume fraction below control (0.46 +/- 0.23 vs. 0.73 +/- 0.13%, P < or = 0.05). These findings indicate that estrogen's cardioprotective role can be partially mediated by its effects on cardiac mast cells, MMPs, and the extracellular matrix.
机译：男性和女性在心脏病易感性方面存在根本差异。尽管许多心力衰竭动物模型已经证明，绝经前的雌性具有心脏保护作用，因此面对心脏病时的抵抗力要好于雄性，但仍然存在许多有关如何发生这种情况的问题。最近，我们发现1）肥大细胞密度增加与不良的心室重构相关; 2）使用化合物48/80化学诱导的肥大细胞脱粒导致基质金属蛋白酶（MMP）活性，心脏胶原结构和心脏舒张功能发生显着变化在正常的雄性大鼠中。考虑到已知的心脏病性别差异，我们试图检查化学诱导的心脏肥大细胞脱粒对完整雌性大鼠，去卵巢雌性大鼠和接受17β-雌二醇治疗的去卵巢雌性大鼠的离体，血液灌注心脏的影响。响应肥大细胞脱粒，在完整雌性大鼠和经雌激素处理的卵巢切除雌性大鼠之间，在心脏功能，MMP-2活性或胶原蛋白体积分数方面均未观察到显着差异。在经卵巢切除的女性组中，用化合物48/80治疗后，注意到左心室压力-容积关系有明显的向右移动，同时活性MMP-2值比完整女性组显着增加133％（ P <或= 0.05），以及胶原蛋白体积分数显着低于对照（0.46 +/- 0.23对0.73 +/- 0.13％，P <或= 0.05）。这些发现表明，雌激素的心脏保护作用可以部分通过其对心脏肥大细胞，MMP和细胞外基质的作用来介导。

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