Oxidative stress-inducible protein tyrosine phosphatase in glomerulonephritis.

Authors: Feng, L  Xia, Y  Seiffert, D  Wilson, CB 
Citation: Feng L, etal., Kidney Int 1995 Dec;48(6):1920-8.
Pubmed: (View Article at PubMed) PMID:8587253

Previously we found that rat mesangial cells express 3CH134/CL100 protein-tyrosine phosphatase (PTPase) in response to reactive oxygen intermediates (ROIs), and we now extend these studies to glomerulonephritis (GN), where ROI have been demonstrated to play a role. The rat homologue of 3CH134/CL100 was cloned from a rat macrophage cDNA library. The rat 3CH134/CL100 mRNA was strongly induced in the lung, liver, and heart the first day after birth, suggesting that hyperoxic adaption might be involved in the induction of the PTPase mRNA. In anti-glomerular basement membrane (GBM) antibody (Ab) GN in rats, the 3CH134/CL100 PTPase mRNA was expressed in glomeruli as early as 30 minutes after anti-GBM Ab injection. The 3CH134/CL100 mRNA expression was modulated by the ROI scavenger dimethylthiourea (DMTU), indicating that its induction was ROI related. In contrast to the glomerular lesion, PTPase mRNA expression was not induced in experimental tubulointerstitial nephritis. In situ hybridization suggested that mesangial and some infiltrating cells were the major glomerular cell sources of the PTPase mRNA. These results indicate that rat CCH134/CL100 PTPase is actively induced in glomeruli as part of an acute immune injury at least in part related to oxidative stress. PTPase induction in GN and potentially other forms of inflammation may play an important regulatory role in protein kinase signaling pathways.

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CRRD Object Information
CRRD ID: 633769
Created: 2003-08-29
Species: All species
Last Modified: 2004-05-25
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.