Anti-GBM glomerulonephritis in mice lacking nitric oxide synthase type 2 Rapid Communication View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1998-04

AUTHORS

V Cattell, H T Cook, H Ebrahim, S N Waddington, X Q Wei, K J Assmann, F Y Liew

ABSTRACT

Nitric oxide is synthesized in experimental immune complex glomerulonephritis due to local induction of type 2 nitric oxide synthase (NOS2). To determine the role of NOS2, the course of accelerated anti-glomerular basement membrane glomerulonephritis (anti-GBM) was examined in mice homozygous for disruption of the NOS2 gene compared with heterozygous littermates. Disease in the wild type strain (129Sv) was characterized by heavy albuminuria, glomerular neutrophil and macrophage infiltration and glomerular thrombosis. NOS2, interleukin 1B (IL-1 beta) and tumor necrosis factor alpha (TNF alpha) mRNA were induced by 24 hours. The NOS2-deficient mutant mice and the heterozygous mice displayed early (24 hr) and full autologous phase (day 6) injury indistinguishable from the wild-type mice. The equivalent degree of albuminuria and glomerular inflammation indicates that NOS2 does not play an essential role in this form of glomerulonephritis in the mouse. More... »

PAGES

932-936

Identifiers

URI

http://scigraph.springernature.com/pub.10.1111/j.1523-1755.1998.00892.x

DOI

http://dx.doi.org/10.1111/j.1523-1755.1998.00892.x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1046268114

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9551400


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