S P Makker1, R Widstrom, J Huang. 1. Department of Pediatrics, School of Medicine University of California-Davis 95817, USA.
Abstract
UNLABELLED: Active Heymann nephritis (HN) of rat, an autoimmune glomerular disease, is a model for human membranous glomerulonephropathy. The autoantigen of HN is a glycoprotein of approximately 600 kd that is present in both rat and human kidneys. Another kidney protein of 39-45 kd called receptor-associated protein (RAP) is associated with gp600. In normal kidney very little gp600 and RAP can be detected in glomeruli. This study was undertaken to determine whether the synthesis of gp600 and RAP would increase after development of active HN. Kidneys from normal (n = 5) and active (n = 11) HN rats were studied for expression of gp600 and RAP and their mRNAs by immunofluorescence and in situ hybridization. In all HN kidneys in contrast to normal kidneys both the transcription and translation of gp600 were markedly increased in glomeruli and proximal tubules. Transcription and translation of RAP were also increased but less so than gp600. The site of increased transcription of gp600 and RAP in glomeruli was clearly localized to the visceral glomerular epithelial cells. CONCLUSIONS: This is the first study to show increased transcription of gp600 and RAP in active HN and the first study to identify the visceral glomerular epithelial cell as the cell for the increased transcription.
UNLABELLED: Active Heymann nephritis (HN) of rat, an autoimmune glomerular disease, is a model for humanmembranous glomerulonephropathy. The autoantigen of HN is a glycoprotein of approximately 600 kd that is present in both rat and human kidneys. Another kidney protein of 39-45 kd called receptor-associated protein (RAP) is associated with gp600. In normal kidney very little gp600 and RAP can be detected in glomeruli. This study was undertaken to determine whether the synthesis of gp600 and RAP would increase after development of active HN. Kidneys from normal (n = 5) and active (n = 11) HN rats were studied for expression of gp600 and RAP and their mRNAs by immunofluorescence and in situ hybridization. In all HN kidneys in contrast to normal kidneys both the transcription and translation of gp600 were markedly increased in glomeruli and proximal tubules. Transcription and translation of RAP were also increased but less so than gp600. The site of increased transcription of gp600 and RAP in glomeruli was clearly localized to the visceral glomerular epithelial cells. CONCLUSIONS: This is the first study to show increased transcription of gp600 and RAP in active HN and the first study to identify the visceral glomerular epithelial cell as the cell for the increased transcription.