Expression profiles of fibrinolytic components in nasal mucosa
Expression profiles of fibrinolytic components in nasal mucosa
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DOI：
10.1007/s00418-004-0664-2
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发表时间：
2004-06
影响因子：
2.3
通讯作者：
Takayuki Sejima;S. Madoiwa;J. Mimuro;T. Sugo;T. Ishida;K. Ichimura;Y. Sakata
中科院分区：
文献类型：
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作者：
Takayuki Sejima;S. Madoiwa;J. Mimuro;T. Sugo;T. Ishida;K. Ichimura;Y. Sakata
纤维蛋白溶解途径的组分除了在纤维蛋白凝块降解中的公认作用之外，还在许多组织中促进不同的途径。在这项研究中的鼻粘膜，我们调查的组织型纤溶酶原激活剂（t-PA），尿激酶型纤溶酶原激活剂（u-PA），纤溶酶原激活剂抑制剂-1（派-1），纤溶酶原激活剂抑制剂-2（派-2）的mRNA的存在下，使用逆转录聚合酶链反应（RT-PCR）和原位杂交，并比较这些结果与它们在免疫组织中的定位。实时荧光定量RT-PCR结果显示，t-PA、u-PA、派-1和派-2 mRNA在人鼻粘膜中均有表达。特别是u-PA和派-1 mRNA的表达在变应性鼻粘膜中显著高于正常粘膜。t-PA mRNA在正常鼻粘膜内皮细胞和上皮细胞中均有表达。t-PA mRNA在变态反应粘膜下腺体粘液细胞中表达，而在正常腺体中未表达。在变应性鼻炎中，u-PA和派-2 mRNA表达于粘液细胞和上皮细胞，派-1 mRNA表达于浆液细胞和上皮细胞。u-PA和派-1 mRNA在正常鼻组织中的表达低于变应性鼻组织。u-PA染色见于变应性粘膜下腺体粘液细胞，派-2的染色模式与u-PA相似。派-1存在于过敏样品的粘膜下腺体的浆液细胞中，而上皮细胞几乎没有染色。与此相反，过敏，组织-PA免疫组化染色是阴性的粘膜下腺体，虽然在内皮细胞和上皮细胞阳性。变应性鼻炎鼻粘膜组织中t-PA mRNA的表达主要在粘膜细胞中。鼻分泌物纤维蛋白自显影中，u-PA在过敏患者中明显激活。这些结果表明，t-PA合成的粘液细胞迅速分泌和修改水样鼻分泌物在变应性鼻炎，u-PA活性可能有助于通过大量的鼻分泌物也降低其粘度。变应性鼻粘膜可见大量细胞浸润，尤其是嗜酸性粒细胞浸润。PA和PAI表达的改变很可能是由于这些炎症和免疫细胞局部释放细胞因子或生长因子所致。
Components of the fibrinolytic pathway contribute to diverse pathways in many tissues, in addition to their well-recognized role in degradation of fibrin clots. In this study of nasal mucosa, we investigated the presence of mRNA of tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), plasminogen activator inhibitor-1 (PAI-1), and plasminogen activator inhibitor-2 (PAI-2) using reverse transcription polymerase chain reaction (RT-PCR) and in situ hybridization, and compared these results with their localization in immunostained tissues. According to real-time RT-PCR results, t-PA, u-PA, PAI-1, and PAI-2 mRNA were noted in human nasal mucosa. Particularly, expression of u-PA and PAI-1 mRNA was significantly high in allergic nasal mucosa in comparison with normal mucosa. t-PA mRNA was detected in endothelial cells and epithelium in normal nasal mucosa. t-PA mRNA was detected in mucous cells of allergic submucosal glands, but not in normal glands. In allergic rhinitis, u-PA and PAI-2 mRNA were detected in mucinous cells and epithelium, and PAI-1 mRNA was detected in serous cells and epithelium. Expression of u-PA and PAI-1 mRNA in normal nasal tissues was decreased in contrast to that in allergic nasal tissues. u-PA staining was observed in mucous cells of allergic submucosal glands and the staining pattern of PAI-2 was similar to that of u-PA. PAI-1 was present in serous cells of submucosal glands from allergy samples, while epithelial cells were almost devoid of stain. In contrast, with allergy, immunohistochemical staining of t-PA was negative in submucosal glands, though positive in endothelial cells and epithelium. However, the expression of t-PA mRNA in allergic nasal mucosa was noted in mucous cells. In fibrin autography of nasal discharge, u-PA was markedly activated in the allergic patient. These results suggest that t-PA synthesized in mucous cells is promptly secreted and modifies watery nasal discharge in allergic rhinitis, and that u-PA activity may help the passage of large amounts of rhinorrhea by also reducing its viscosity. A lot of cellular infiltration (eosinophils in particular) was recognized in allergic nasal mucosa. It is most likely that the modifications in expression of PAs and PAIs are due to the local release of cytokines or growth factors from these inflammatory and immune cells.