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首页> 外文期刊>American Journal of Physiology >Negative impact of tissue inhibitor of metalloproteinase-3 null mutation on lung structure and function in response to sepsis.
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Negative impact of tissue inhibitor of metalloproteinase-3 null mutation on lung structure and function in response to sepsis.

机译：组织蛋白酶金属蛋白酶3无效突变对败血症反应对肺结构和功能的负面影响。

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摘要

Matrix metalloproteinases (MMPs) are degradative enzymes, which act to remodel tissue. Their activity is regulated by the tissue inhibitors of metalloproteinases (TIMPs). An imbalance in the degradation/inhibition activities has been associated with many diseases, including sepsis. We have previously shown that TIMP-3 knockout animals develop spontaneous, progressive air space enlargement. The objectives of this study were to determine the effects of a septic lung stress induced by cecal ligation and perforation (CLP) on lung function, structure, pulmonary surfactant, and inflammation in TIMP-3 null mice. Knockout and wild-type animals were randomized to either sham or CLP surgery, allowed to recover for 6 h, and then euthanized. TIMP-3 null animals exposed to sham surgery had a significant increase in lung compliance when compared with sham wild-type mice. Additionally, the TIMP-3 knockout mice showed a significant increase in compliance following CLP. Rapid compliance changes were accompanied by significantly decreased collagen and fibronectin levels and increased gelatinase (MMP-2 and -9) abundance and activation. Additionally, in situ zymography showed increased airway-associated gelatinase activity in the knockout animals enhanced following CLP. In conclusion, exposing TIMP-3 null animals to sepsis rapidly enhances the phenotypic abnormalities of these mice, due to increased MMP activity induced by CLP.
机译：基质金属蛋白酶（MMP）是降解酶，可重塑组织。它们的活性由金属蛋白酶（TIMPs）的组织抑制剂调节。降解/抑制活性的失衡与包括败血症在内的许多疾病有关。先前我们已经证明TIMP-3基因敲除动物会自发进行性气隙扩大。这项研究的目的是确定盲肠结扎和穿孔（CLP）引起的败血症性肺应激对TIMP-3缺失小鼠肺功能，结构，肺表面活性剂和炎症的影响。剔除和野生型动物随机接受假手术或CLP手术，恢复6小时，然后安乐死。与假野生型小鼠相比，接受假手术的TIMP-3无效动物的肺顺应性显着提高。此外，TIMP-3敲除小鼠在CLP后显示顺应性显着增加。快速顺应性变化伴随着胶原蛋白和纤连蛋白水平的显着降低以及明胶酶（MMP-2和-9）的丰度和活化增加。此外，原位酶谱分析显示，CLP后基因敲除动物的气道相关明胶酶活性增加。总之，由于CLP诱导的MMP活性增加，使TIMP-3无效动物暴露于败血症会迅速增强这些小鼠的表型异常。

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