Electronic Resource

Plasminogen and plasminogen activators protect against renal injury in crescentic glomerulonephritis.

التفاصيل البيبلوغرافية
العنوان: Plasminogen and plasminogen activators protect against renal injury in crescentic glomerulonephritis.
المؤلفون: Plow E.F., Tipping P.G., Ploplis V.A., Collen D., Holdsworth S.R., Carmeliet P., Richard Kitching A.R.
بيانات النشر: Rockefeller University Press (1114 First Avenue, 4th Floor, New York NY 10021-8325, United States) United States 2012-10-22
نوع الوثيقة: Electronic Resource
مستخلص: The plasminogen/plasmin system has the potential to affect the outcome of inflammatory diseases by regulating accumulation of fibrin and other matrix proteins. In human and experimental crescentic glomerulonephritis (GN), fibrin is an important mediator of glomerular injury and renal impairment. Glomerular deposition of matrix proteins is a feature of progressive disease. To study the role of plasminogen and plasminogen activators in the development of inflammatory glomerular injury, GN was induced in mice in which the genes for these proteins had been disrupted by homologous recombination. Deficiency of plasminogen or combined deficiency of tissue type plasminogen activator (tPA) and urokinase type plasminogen activator (uPA) was associated with severe functional and histological exacerbation of glomerular injury. Deficiency of tPA, the predominant plasminogen activator expressed in glomeruli, also exacerbated disease. uPA deficiency reduced glomerular macrophage infiltration and did not significantly exacerbate disease. uPA receptor deficiency did not effect the expression of GN. These studies demonstrate that plasminogen plays an important role in protecting the glomerulus from acute inflammatory injury and that tPA is the major protective plasminogen activator.
مصطلحات الفهرس: cell protection, controlled study, female, glomerulonephritis/et [Etiology], glomerulus filtration, histopathology, macrophage activation, male, mouse, nonhuman, pathophysiology, plasminogen activation, priority journal, animal cell, fibrin, plasminogen, plasminogen activator, tissue plasminogen activator, urokinase, animal model, receptor binding, animal tissue, article, Article
URL: https://repository.monashhealth.org/monashhealthjspui/handle/1/33863
Click here for full text options
LibKey Link
الاتاحة: Open access content. Open access content
Copyright 2012 Elsevier B.V., All rights reserved.
Other Numbers: AUSHL oai:repository.monashhealth.org:1/33863
Journal of Experimental Medicine. 185 (5) (pp 963-968), 1997. Date of Publication: 1997.
0022-1007
https://repository.monashhealth.org/monashhealthjspui/handle/1/33863
9120402 [http://www.ncbi.nlm.nih.gov/pubmed/?term=9120402]
27119880
(Richard Kitching, Holdsworth, Tipping) Department of Medicine, Center for Inflammatory Diseases, Monash University, 3168, Victoria, Australia (Richard Kitching, Collen, Carmeliet) Ctr. Transgene Technol./Gene Therapy, Vlaams Interuniv. Inst. Biotech., B-3000 Leuven, Belgium (Ploplis) Joseph J. Jacobs Ctr. Thromb./V.B., Cleveland, OH 44195, United States (Plow) Monash University, Department of Medicine, Monash Medical Centre, 246 Clayton Road, Clayton, Vic. 3168, Australia
1305135386
المصدر المساهم: MONASH HEALTH LIBRS
From OAIster®, provided by the OCLC Cooperative.
رقم الانضمام: edsoai.on1305135386
قاعدة البيانات: OAIster