Experimental Glomerulonephritis

Several animal models including rat and mice model are currently used in our laboratory for the exploring of pathogenesis and genetic susceptibility of glomerulonephritis. Recently, by using crescentic glomerulonephritis induced in WKY rat, we found that the susceptibility of WKY rat to crescentic glomerulonephritis is related to both glomerular intrinsic cell and bone marrow derived immune cells. Moreover, glomerular intrinsic cell play a even more important role than circulating immune cells in the formation of crescentic glomerulonephritis. This result demonstrates that although susceptibility of crescentic glomerulonephritis in WKY is determined by gene, i.e. Fc III as shown by Aitman TJ ( Aitman TJ Nature Feb, p851-5, 2006). The renal intrinsic factor can still modify its phenotype. This result was published in Journal of American Society of Nephrology June, 2007 (JASN, June p1816-23).

Our previous studies, using MRL/lpr and NZB/NZW lupus mice, also demonstrate that aminoguanidine reduces glomerular inducible nitric oxide synthase (iNOS) and transforming growth factor-beta 1 (TGF-beta1) mRNA expression and diminishes glomerulosclerosis in NZB/W F1 mice (Clin Exp Immunol. 1998 Aug;113(2):258-64). Furthermore, mycophenolate mofetil reduces renal cortical inducible nitric oxide synthase mRNA expression and diminishes glomerulosclerosis in MRL/lpr mice (J Lab Clin Med. 2001 Jul;138(1):69-77).