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[尿激酶型纤溶酶原激活剂在天疱疮发病机制中的作用]

[The role of urokinase-type plasminogen activator in the pathogenesis of pemphigus].

作者信息

Nie Z, Liu R, Ye Q

机构信息

Department of Dermatology, Southwest Hospital Third Military Medical University, Chongquing.

出版信息

Zhonghua Yi Xue Za Zhi. 1997 Oct;77(10):771-3.

PMID:9772525
Abstract

OBJECTIVE

To investigate the changes of urokinase-type plasmino-gen activator (u-PA) in the process of acantholysis in pemphigus and observe the influence of purified urokinase on the cultured skin explant.

METHODS

The expression of urokinase antigen on the pemphigus organ model was revealed by immunohistochemical method; PA activity was assayed in the acantholysis model; the influence of urokinase on the epidermis was observed by adding purified urokinase into the cultured skin explant.

RESULTS

PA activity was elevated in the acantholysis model at 24 hour and was continuing its increase at 48 and 72 hours. The expression of urokinase was high in the epidermis of pemphigus organ model; purified urokinase could induce acantholysis like changes.

CONCLUSION

Pemphigus antibody induces acantholysis through activating keratinocytes. The latter secretes an elevated u-PA, which locates on the membrane of the epidermal cells producing a limited pro-teolysis which damages the cohesion of epidermal cells.

摘要

目的

研究天疱疮棘层松解过程中尿激酶型纤溶酶原激活剂(u-PA)的变化,并观察纯化尿激酶对培养皮肤外植体的影响。

方法

采用免疫组化方法检测天疱疮器官模型中尿激酶抗原的表达;在棘层松解模型中测定纤溶酶原激活剂(PA)活性;将纯化尿激酶加入培养的皮肤外植体中,观察尿激酶对表皮的影响。

结果

棘层松解模型在24小时时PA活性升高,48小时和72小时时持续升高。天疱疮器官模型表皮中尿激酶表达较高;纯化尿激酶可诱导类似棘层松解的变化。

结论

天疱疮抗体通过激活角质形成细胞诱导棘层松解。后者分泌升高的u-PA,其定位于表皮细胞膜上,产生有限的蛋白水解作用,破坏表皮细胞的黏附力。

相似文献

1
[The role of urokinase-type plasminogen activator in the pathogenesis of pemphigus].[尿激酶型纤溶酶原激活剂在天疱疮发病机制中的作用]
Zhonghua Yi Xue Za Zhi. 1997 Oct;77(10):771-3.
2
Involvement of urokinase-type plasminogen activator in acantholysis induced by pemphigus IgG.尿激酶型纤溶酶原激活剂在天疱疮IgG诱导的棘层松解中的作用。
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Functional involvement of urokinase-type plasminogen activator receptor in pemphigus acantholysis.尿激酶型纤溶酶原激活物受体在天疱疮棘层松解中的功能作用。
J Cutan Pathol. 1998 Oct;25(9):469-74. doi: 10.1111/j.1600-0560.1998.tb01777.x.
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Dexamethasone inhibits plasminogen activator activity in experimental pemphigus in vivo but does not block acantholysis.地塞米松在体内实验性天疱疮中抑制纤溶酶原激活物活性,但不阻止棘层松解。
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Role of plasminogen activator in pemphigus vulgaris.纤溶酶原激活剂在寻常型天疱疮中的作用。
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No activation of urokinase plasminogen activator by anti-desmoglein 3 monoclonal IgG antibodies in cultured human keratinocytes.在培养的人角质形成细胞中,抗桥粒芯糖蛋白3单克隆IgG抗体不会激活尿激酶型纤溶酶原激活剂。
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7
Protease inhibitors prevent plasminogen-mediated, but not pemphigus vulgaris-induced, acantholysis in human epidermis.蛋白酶抑制剂可阻止人表皮中纤溶酶原介导的棘层松解,但不能阻止寻常型天疱疮诱导的棘层松解。
Biol Chem. 2003 Feb;384(2):311-5. doi: 10.1515/BC.2003.035.
8
Characterization of keratinocyte plasminogen activator inhibitors and demonstration of the prevention of pemphigus IgG-induced acantholysis by a purified plasminogen activator inhibitor.角质形成细胞纤溶酶原激活物抑制剂的特性及一种纯化的纤溶酶原激活物抑制剂预防天疱疮IgG诱导的棘层松解的证明
J Invest Dermatol. 1989 Mar;92(3):310-4. doi: 10.1111/1523-1747.ep12277087.
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Pemphigus IgG induces expression of urokinase plasminogen activator receptor on the cell surface of cultured keratinocytes.天疱疮IgG可诱导培养的角质形成细胞表面尿激酶型纤溶酶原激活物受体的表达。
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Imbalance between plasminogen activator and its inhibitors in thiol-induced acantholysis.硫醇诱导的棘层松解中纤溶酶原激活物与其抑制剂之间的失衡。
Dermatology. 1993;186(2):118-22. doi: 10.1159/000247321.