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Plasminogen activator inhibitor type 2 is expressed in keratinocytes during re-epithelialization of epidermal defects.

作者信息

Bechtel M J, Wysocki N S, Heidtmann A, Stark H J, Fusenig N, Kramer M D, Schaefer B M

机构信息

University Institute for Immunology, Laboratory for Immunopathology, Heidelberg, Germany.

出版信息

Br J Dermatol. 1998 Jan;138(1):22-8. doi: 10.1046/j.1365-2133.1998.02021.x.

DOI:10.1046/j.1365-2133.1998.02021.x
PMID:9536219
Abstract

Plasminogen activation is observed in the human epidermis during re-epithelialization of epidermal defects. The activation reaction depends on plasminogen activators (PAs) associated with re-epithelializing keratinocytes. PA inhibitor type 2 (PAI-2) is thought to be a major epidermal PA inhibitor in keratinocytes. However, no data are available on the expression of PAI-2 in keratinocytes during epidermal regeneration. We have therefore analysed PAI-2 at the mRNA and protein level in keratinocyte cultures as well as in epidermal lesions in which re-epithelializing keratinocytes were apparent. We found that PAI-2 expression at the mRNA and protein level was negatively correlated with the cell density in regular keratinocyte cultures. In organotypic cocultures, in which the transition from a re-epithelializing to a sedentary phenotype can be studied, PAI-2 was most strongly expressed in early cultures prior to formation of a differentiated epidermis-like structure. We found a strong expression of PAI-2 in keratinocytes that re-epithelialized dermal burn wounds or lesions caused by the autoimmune blistering disease pemphigus vulgaris. Our results suggest that not only PAs, but also a major PA inhibitor, PAI-2, are expressed in keratinocytes that are actively involved in re-epithelialization.

摘要

相似文献

1
Plasminogen activator inhibitor type 2 is expressed in keratinocytes during re-epithelialization of epidermal defects.
Br J Dermatol. 1998 Jan;138(1):22-8. doi: 10.1046/j.1365-2133.1998.02021.x.
2
Differential expression of urokinase-type plasminogen activator (uPA), its receptor (uPA-R), and inhibitor type-2 (PAI-2) during differentiation of keratinocytes in an organotypic coculture system.在器官型共培养系统中角质形成细胞分化过程中尿激酶型纤溶酶原激活剂(uPA)、其受体(uPA-R)和2型抑制剂(PAI-2)的差异表达。
Exp Cell Res. 1995 Oct;220(2):415-23. doi: 10.1006/excr.1995.1333.
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Plasminogen activator inhibitor 2: expression and role in differentiation of epidermal keratinocyte.纤溶酶原激活物抑制剂2:在表皮角质形成细胞分化中的表达及作用
Biol Cell. 2004 Mar;96(2):109-16. doi: 10.1016/j.biolcel.2003.09.007.
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Retinoic acid upregulates the plasminogen activator system in human epidermal keratinocytes.维甲酸上调人表皮角质形成细胞中的纤溶酶原激活物系统。
J Invest Dermatol. 2001 May;116(5):778-84. doi: 10.1046/j.1523-1747.2001.01310.x.
5
Overexpression of plasminogen activator inhibitor type 2 in basal keratinocytes enhances papilloma formation in transgenic mice.基底角质形成细胞中纤溶酶原激活物抑制剂2的过表达增强转基因小鼠乳头瘤的形成。
Cancer Res. 2001 Feb 1;61(3):970-6.
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Hydrocortisone regulates the dynamics of plasminogen activator and plasminogen activator inhibitor expression in cultured murine keratinocytes.氢化可的松调节培养的小鼠角质形成细胞中纤溶酶原激活物和纤溶酶原激活物抑制剂表达的动态变化。
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7
Plasminogen activator inhibitor type-2 (PAI-2) in human keratinocytes regulates pericellular urokinase-type plasminogen activator.人类角质形成细胞中的2型纤溶酶原激活物抑制剂(PAI-2)调节细胞周围尿激酶型纤溶酶原激活物。
Exp Cell Res. 1996 Feb 25;223(1):91-101. doi: 10.1006/excr.1996.0061.
8
mRNA for tissue-type plasminogen activator is present in lesional epidermis from patients with psoriasis, pemphigus, or bullous pemphigoid, but is not detected in normal epidermis.组织型纤溶酶原激活剂的信使核糖核酸存在于银屑病、天疱疮或大疱性类天疱疮患者的皮损表皮中,但在正常表皮中未检测到。
J Invest Dermatol. 1990 Nov;95(5):548-52. doi: 10.1111/1523-1747.ep12504901.
9
Evidence for intracellular cleavage of plasminogen activator inhibitor type 2 (PAI-2) in normal epidermal keratinocytes.正常表皮角质形成细胞中纤溶酶原激活物抑制剂2(PAI-2)细胞内裂解的证据。
J Cell Physiol. 2000 Feb;182(2):281-9. doi: 10.1002/(SICI)1097-4652(200002)182:2<281::AID-JCP17>3.0.CO;2-D.
10
Calcium modulates the expression of urokinase plasminogen activator and plasminogen activator inhibitor 2 by human keratinocytes.
Exp Dermatol. 1994 Apr;3(2):85-8. doi: 10.1111/j.1600-0625.1994.tb00052.x.

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