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Originally published online as doi:10.2353/ajpath.2009.080476 on February 26, 2009

Published online before print February 26, 2009
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(American Journal of Pathology. 2009;174:1368-1378.)
© 2009 American Society for Investigative Pathology
DOI: 10.2353/ajpath.2009.080476

Anti-Inflammatory and Renal Protective Actions of Stanniocalcin-1 in a Model of Anti-Glomerular Basement Membrane Glomerulonephritis

Luping Huang*, Gabriela Garcia*, Yahuan Lou{dagger}, Qin Zhou{dagger}, Luan D. Truong{ddagger}, Gabriel DiMattia§, Xia Ru Lan||, Hui Y. Lan||, Yanlin Wang* and David Sheikh-Hamad*

From the Division of Nephrology,* Department of Medicine, Baylor College of Medicine, Houston, Texas; the Dental Branch,{dagger} University of Texas Health Science Center, Houston, Texas; the Department of Pathology and Laboratory Medicine,{ddagger} Weill Medical College of Cornell University, New York, New York; the Departments of Oncology,§ and Biochemistry, London Regional Cancer Center, University of Western Ontario, London, Ontario, Canada; and the Department of Medicine,|| The University of Hong Kong, Hong Kong, People’s Republic of China

We have previously shown that stanniocalcin-1 (STC1) inhibits the transendothelial migration of macrophages and T cells, suppresses superoxide generation in macrophages, and attenuates macrophage responses to chemoattractants. To study the effects of STC1 on inflammation, in this study we induced a macrophage- and T-cell-mediated model of anti-glomerular basement membrane disease in STC1 transgenic mice, which display elevated serum STC1 levels and preferentially express STC1 in both endothelial cells and macrophages. We examined the following parameters both at baseline and after anti-glomerular basement membrane antibody treatment: blood pressure; C3a levels; urine output; proteinuria; blood urea nitrogen; and kidney C3 deposition, fibrosis, histological changes, cytokine expression, and number of T cells and macrophages. Compared with wild-type mice, after anti-glomerular basement membrane treatment STC1 transgenic mice exhibited: i) diminished infiltration of inflammatory macrophages in the glomeruli; ii) marked reduction in crescent formation and sclerotic glomeruli; iii) decreased interstitial fibrosis; iv) preservation of kidney function and lower blood pressure; v) diminished C3 deposition in the glomeruli; and vi) reduced expression of macrophage inhibitory protein-2 and transforming growth factor-β2 in the kidney. Compared with baseline, wild-type mice, but not STC1 transgenic mice, had higher proteinuria and a marked reduction in urine output. STC1 had minimal effects, however, on both T-cell number in the glomeruli and interstitium and on cytokine expression characteristic of either TH1 or TH2 activation. These data suggest that STC1 is a potent anti-inflammatory and renal protective protein.




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