We infused microgram quantities of active or inactive PMN elastase and cathepsin G into the renal arteries of rats. Both active and inactive elastase localized to the glomerular capillary wall equally, and in amounts that could be achieved physiologically in GN. However, elastase-perfused rats developed marked proteinuria (196 +/- 32 mg/24 h) compared with control rats receiving inactive elastase (19 +/- 2 mg/24 h, p less than 0.005). Similar results were seen with active and inactive cathepsin G. Neither elastase nor cathepsin G infusion was associated with histologic evidence of glomerular injury. We conclude that the PMN neutral serine proteinases elastase and cathepsin G can mediate marked changes in glomerular permeability in vivo due to their proteolytic activity, and thus, may contribute to the proteinuria observed in PMN-dependent models of GN.
The human neutrophil serine proteinases, elastase and cathepsin G, can mediate glomerular injury in vivo.
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R J Johnson, W G Couser, C E Alpers, M Vissers, M Schulze, S J Klebanoff; The human neutrophil serine proteinases, elastase and cathepsin G, can mediate glomerular injury in vivo.. J Exp Med 1 September 1988; 168 (3): 1169–1174. doi: https://doi.org/10.1084/jem.168.3.1169
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