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Publication Detail
Arginase activity is modulated by IL-4 and HOArg in nephritic glomeruli and mesangial cells
  • Publication Type:
    Journal article
  • Publication Sub Type:
    JOUR
  • Authors:
    Waddington SN, Tam FWK, Cook HT, Cattell V
  • Publication date:
    1998
  • Pagination:
    F473, F480
  • Volume:
    274
  • Issue:
    3
  • Notes:
    Arginase shares a common substrate, L-arginine, with nitric oxide synthase (NOS). Both enzymes are active at inflammatory sites. To understand regulation of arginase and its relationship to NO production we studied effects of NG-hydroxy-L-arginine (HOArg) and IL-4 on urea and nitrite (NO2-) synthesis by glomeruli during rat immune glomerulonephritis and compared these with macrophages and glomerular mesangial cells (MC). In nephritic glomeruli, elicited macrophages, and MC stimulated with IL-1 and cAMP agonists, the following pattern was found: there was increased arginase and induced NOS activity. Urea production was inhibited by HOArg and increased by IL-4. NO inhibition (NG-monomethyl-L-arginine, L-NMMA) increased arginase activity in nephritic glomeruli and macrophages but not MC. NO2- synthesis was inhibited by L-NMMA and IL-4. It was increased with HOArg under conditions of NO inhibition. In contrast, in normal glomeruli and basal MC, where there was no induced NO synthesis, IL-4 had no effect on arginase activity, while HOArg consistently reduced it in glomeruli only. This is the first demonstration of arginase modulation in glomeruli and MC. The differential responses to two endogenous compounds generated by inflammation suggest this may be part of co-ordinated regulation of arginase and iNOS in immune injury, whereby arginase is inhibited during high output NO production, and stimulated with NO suppression. This may be important in controlling the balance of inflammatory and repair mechanisms.
Abstract
Arginase shares a common substrate, L-arginine, with nitric oxide synthase (NOS). Both enzymes are active at inflammatory sites. To understand regulation of arginase and its relationship to NO production we studied effects of NG-hydroxy-L-arginine (HOArg) and IL-4 on urea and nitrite (NO2-) synthesis by glomeruli during rat immune glomerulonephritis and compared these with macrophages and glomerular mesangial cells (MC). In nephritic glomeruli, elicited macrophages, and MC stimulated with IL-1 and cAMP agonists, the following pattern was found: there was increased arginase and induced NOS activity. Urea production was inhibited by HOArg and increased by IL-4. NO inhibition (NG-monomethyl-L-arginine, L-NMMA) increased arginase activity in nephritic glomeruli and macrophages but not MC. NO2- synthesis was inhibited by L-NMMA and IL-4. It was increased with HOArg under conditions of NO inhibition. In contrast, in normal glomeruli and basal MC, where there was no induced NO synthesis, IL-4 had no effect on arginase activity, while HOArg consistently reduced it in glomeruli only. This is the first demonstration of arginase modulation in glomeruli and MC. The differential responses to two endogenous compounds generated by inflammation suggest this may be part of co-ordinated regulation of arginase and iNOS in immune injury, whereby arginase is inhibited during high output NO production, and stimulated with NO suppression. This may be important in controlling the balance of inflammatory and repair mechanisms.
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