Anti-GBM glomerulonephritis in mice lacking nitric oxide synthase type 2

Cattell, V., Cook, H. T., Ebrahim, H. B., Waddington, S. N., Wei, Xiao-Qing ORCID: https://orcid.org/0000-0002-6274-8503, Assmann, K. J. M. and Liew, Foo Y. 1998. Anti-GBM glomerulonephritis in mice lacking nitric oxide synthase type 2. Kidney International 53 (4) , pp. 932-936.

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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.

Item Type:	Article
Date Type:	Publication
Status:	Published
Schools:	Dentistry
Subjects:	R Medicine > RK Dentistry
Publisher:	Nature Publishing Group
ISSN:	0085-2538
Last Modified:	21 Oct 2022 09:13
URI:	https://orca.cardiff.ac.uk/id/eprint/35655

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