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Anti-GBM glomerulonephritis in mice lacking nitric oxide synthase type 2
V Cattell1, H T Cook, H Ebrahim
1Department of Histopathology, Imperial College School of Medicine, London, England, United Kingdom.
Kidney International
|April 29, 1998
Summary
Type 2 nitric oxide synthase (NOS2) is induced in experimental glomerulonephritis. However, NOS2-deficient mice showed no difference in disease severity, indicating NOS2 is not essential for this kidney inflammation model.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Nitric oxide (NO) is synthesized in experimental immune complex glomerulonephritis.
- This synthesis is linked to the local induction of type 2 nitric oxide synthase (NOS2).
Purpose of the Study:
- To determine the role of NOS2 in accelerated anti-glomerular basement membrane (anti-GBM) glomerulonephritis.
- To investigate the impact of NOS2 deficiency on disease progression and kidney injury.
Main Methods:
- Examined accelerated anti-GBM glomerulonephritis in mice homozygous for NOS2 gene disruption.
- Compared disease course in NOS2-deficient mice with heterozygous littermates and wild-type controls.
- Assessed albuminuria, glomerular immune cell infiltration, and thrombosis.
Main Results:
- NOS2, IL-1 beta, and TNF alpha mRNA were induced within 24 hours in wild-type mice.
- NOS2-deficient and heterozygous mice exhibited indistinguishable early and late-stage kidney injury compared to wild-type.
- Equivalent albuminuria and glomerular inflammation were observed across all groups.
Conclusions:
- NOS2 does not play an essential role in the development of accelerated anti-GBM glomerulonephritis in mice.
- The absence of NOS2 did not alter the severity of kidney injury or inflammation in this experimental model.