ADAM33 is not essential for growth and development and does not modulate allergic asthma in mice
ADAM33 is not essential for growth and development and does not modulate allergic asthma in mice
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DOI：
10.1128/mcb.00646-06
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发表时间：
2006-09-01
影响因子：
5.3
通讯作者：
Sheppard, Dean
中科院分区：
文献类型：
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作者：
Chen, Chun;Huang, Xiaozhu;Sheppard, Dean
解整合素和金属蛋白酶33（ADAM33）是一种跨膜蛋白酶和整合素配体，已被鉴定为哮喘易感基因产物。为了确定ADAM33是否在哺乳动物发育和过敏性气道功能障碍的调节中起重要作用，我们通过基因打靶产生了ADAM33缺失小鼠。ADAM 33基因敲除小鼠以预期的孟德尔比例出生，雄性和雌性发育正常且具有生育能力。在任何组织中均未检测到解剖学或组织学异常。在过敏性哮喘的动物模型中，ADAM33基因敲除小鼠表现出正常的过敏原诱导的气道高反应性、免疫球蛋白E产生、粘液化生和气道炎症。我们的研究结果表明，ADAM33是不是必不可少的生长或繁殖的小鼠，并不调节基线或过敏原诱导的气道反应性。
A disintegrin and metalloprotease 33 (ADAM33) is a transmembrane protease and integrin ligand that has been identified as an asthma susceptibility gene product. To determine whether ADAM33 plays important roles in mammalian development and the modulation of allergic airway dysfunction, we generated ADAM33-null mice by gene targeting. ADAM33-null mice were born at expected Mendelian ratios, and both male and females developed normally and were fertile. No anatomical or histological abnormalities were detected in any tissues. In an animal model of allergic asthma, ADAM33-null mice showed normal allergen-induced airway hyperreactivity, immunoglobulin E production, mucus metaplasia, and airway inflammation. Our results demonstrate that ADAM33 is not essential for growth or reproduction in the mouse and does not modulate baseline or allergen-induced airway responsiveness.