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首页> 外文期刊>Development >Extracellular proteolysis alters tooth development in transgenic mice expressing urokinase-type plasminogen activator in the enamel organ.
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Extracellular proteolysis alters tooth development in transgenic mice expressing urokinase-type plasminogen activator in the enamel organ.

机译：细胞外蛋白水解改变搪瓷器官中表达尿激酶型纤溶酶原激活物的转基因小鼠的牙齿发育。

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摘要

By catalyzing plasmin formation, the urokinase-type plasminogen activator (uPA) can generate widespread extracellular proteolysis and thereby play an important role in physiological and pathological processes. Dysregulated expression of uPA during organogenesis may be a cause of developmental defects. Targeted epithelial expression of a uPA-encoding transgene under the control of the keratin type-5 promoter resulted in enzyme production by the enamel epithelium, which does not normally express uPA, and altered tooth development. The incisors of transgenic mice were fragile, chalky-white and, by scanning electron microscopy, their labial surface appeared granular. This phenotype was attributed to a defect in enamel formation during incisor development, resulting from structural and functional alterations of the ameloblasts that differentiate from the labial enamel epithelium. Immunofluorescence revealed that disorganization of the ameloblast layer was associated with a loss of laminin-5, an extracellular matrix molecule mediating epithelial anchorage. Amelogenin, a key protein in enamel formation, was markedly decreased at the enamel-dentin junction in transgenics, presumably because of an apparent alteration in the polarity of its secretion. In addition, increased levels of active transforming growth factor-beta could be demonstrated in mandibles of transgenic mice. Since the alterations detected could be attributed to uPA catalytic activity, this model provides evidence as to how dysregulated proteolysis, involving uPA or other extracellular proteases, may have developmental consequences such as those leading to enamel defects.
机译：通过催化纤溶酶的形成，尿激酶型纤溶酶原激活剂（uPA）可以产生广泛的细胞外蛋白水解，从而在生理和病理过程中发挥重要作用。在器官发生过程中uPA表达失调可能是发育缺陷的原因。在角蛋白5型启动子的控制下，编码uPA的转基因的靶向上皮表达导致正常上不表达uPA的釉质上皮产生酶，并改变了牙齿发育。转基因小鼠的切牙易碎，呈白色，通过扫描电子显微镜观察，其唇面呈颗粒状。该表型归因于在切牙发育过程中牙釉质形成的缺陷，这是由于成釉细胞与唇釉质上皮细胞不同的结构和功能改变所致。免疫荧光显示成釉细胞层的混乱与层粘连蛋白5的损失有关，层粘连蛋白5是介导上皮锚定的细胞外基质分子。搪瓷形成过程中的关键蛋白-釉蛋白原在转基因产品的釉质-牙本质交界处显着减少，可能是由于其分泌极性的明显改变。另外，在转基因小鼠的下颌骨中可以证明增加水平的活性转化生长因子-β。由于检测到的改变可能归因于uPA的催化活性，因此该模型提供了证据，证明涉及uPA或其他细胞外蛋白酶的蛋白水解失调如何产生发育结果，例如导致牙釉质缺陷的结果。

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