Early activation of metalloproteinases after experimental myocardial infarction occurs in infarct and non-infarct zones

Early activation of metalloproteinases after experimental myocardial infarction occurs in infarct and non-infarct zones
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DOI:
10.1016/s1054-8807(98)00008-8
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发表时间:
1998-11-01
影响因子:
3.7
通讯作者:
Hochman, JS
Hochman, JS
中科院分区:
医学4区
文献类型:
--
作者:
Herzog, E;Gu, AG;Hochman, JS

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心脏的胶原基质形成连接肌纤维、肌束和心肌内血管的网络。心脏中的胶原蛋白周转通常是一个动态过程,涉及胶原蛋白的合成和降解。胶原蛋白分解通常涉及其被基质金属蛋白酶(MMP)的化学消化,所述基质金属蛋白酶在组织修复、伤口愈合和心肌缺血中被激活。我们研究了激活基质金属蛋白酶的酶谱在梗死(前侧壁)和非梗死(隔膜)区大鼠心脏冠状动脉结扎后,以及在假手术大鼠。在梗塞后30分钟、1小时、2小时、4小时和24小时处死大鼠(每个时间段六个心脏)。在不同的分子量下检测到MMP活性,其中54 kDa(MMP-1)、62 kDa(MMP-2)和92 kDa(MMP-9)处的条带最突出。光密度阅读法检测MMP活性。早在梗死后1小时,在MI和远端区中在54 kDa(MMP-1)(p < 0.01)和62 kDa条带(MMP-2)(p < 0.001)处检测到活性,并且在梗死后2小时,在梗死区中仅在92 kDa(MMP-9)处检测到活性(p < 0.05)。MMPs在梗死后早期在梗死区和重要的非梗死区都被激活。这可能导致胶原蛋白分解、梗死扩大和左心室重塑,已知在实验和临床环境中梗死后早期发生。(C)1998年,Elsevier Science Inc.
The collagen matrix of the heart forms a network linking muscle fibers, muscle bundles, and intramyocardial blood vessels. Collagen turnover in the heart is normally a dynamic process that involves both collagen synthesis and degradation. Collagen breakdown generally involves its chemical digestion by matrix metalloproteinases (MMPs) which are activated in tissue repair, wound healing, and myocardial ischemia. We studied activation of MMPs by zymography in infarct (anterolateral wall) and non-infarct (septum) zones of rat hearts following coranary artery ligation, as well as in sham operated rats. Rats were sacrificed at 30 minutes, 1 hour, 2 hours, 4 hours, and 24 hours post infarction (six hearts for each time period). MMP activity was detected at different molecular weights, with bands at 54 kDa (MMP-1), 62 kDa (MMP-2), and 92 kDa (MMP-9) being the most prominent. MMP activities were indexed by densitometer optical reading. Activity was detected as early as 1 hour post infarct in the MI and remote zones at the 54 kDa (MMP-1) (p < 0.01) and 62 kDa bands (MMP-2) (p < 0.001), and at 2 hours post infarct in the infarct zone only at 92 kDa (MMP-9) (p < 0.05). MMPs are activated early after infarction both in the infarct and importantly, non-infarct zones. This may contribute to collagen breakdown, infarct expansion, and left ventricular remodeling, known to occur early after infarction in experimental and clinical settings. (C) 1998 by Elsevier Science Inc.