An immunohistological study of epidermal growth factor receptor and neu receptor and neu receptor expression in proliferative glomerulonephritis

P Roy-Chaudhury, M C Jones, A M MacLeod, N E Haites, J G Simpson, D A Power

Research output: Contribution to journalArticle

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Abstract

Many forms of glomerulonephritis including IgA nephropathy are characterized by mesangial cellular proliferation. Since epidermal growth factor is a potent mitogen for cultured human mesangial cells, we have attempted to localize and quantify the expression of its receptor in normal and abnormal renal biopsies using immunohistochemistry. Using a particular antibody (Amersham, clone EGFR1), the epidermal growth factor receptor (EGF-R) was shown to be predominantly localized in the mesangium of the glomerulus. Visual estimates of intensity of staining suggested that expression of this receptor may be increased in some IgA disease patients with mesangial proliferative glomerular lesions. The neu receptor which has a 50% homology with EGF-R was, however, absent from the glomerulus and cultured mesangial cells did not express detectable levels. Expression of EGF-R by cultured mesangial cells, as assessed by immunostaining, was weak and it was not possible to induce detectable upregulation using different cytokines. The factors leading to increased expression of EGF-R in glomerulonephritis, therefore, remain unknown. Our findings suggest that signalling via EGF-R may play a role in the pathogenesis of proliferative glomerulonephritis. Despite its homology with EGF-R, the neu receptor is unlikely to have similar importance.
Original languageEnglish
Pages (from-to)327-32
Number of pages6
JournalPathology
Volume25
Issue number4
Publication statusPublished - 1 Oct 1993

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ErbB-2 Receptor
Glomerulonephritis
Epidermal Growth Factor Receptor
Mesangial Cells
Immunoglobulin A
Cultured Cells
Mitogens
Epidermal Growth Factor
Up-Regulation
Clone Cells
Immunohistochemistry
Cell Proliferation
epidermal growth factor receptor-neu receptor
Staining and Labeling
Cytokines
Kidney
Biopsy
Antibodies

Keywords

  • Cells, Cultured
  • Glomerular Mesangium
  • Glomerulonephritis, IGA
  • Glomerulonephritis, Membranoproliferative
  • Humans
  • Immunohistochemistry
  • Proto-Oncogene Proteins
  • Receptor, Epidermal Growth Factor
  • Receptor, erbB-2

Cite this

Roy-Chaudhury, P., Jones, M. C., MacLeod, A. M., Haites, N. E., Simpson, J. G., & Power, D. A. (1993). An immunohistological study of epidermal growth factor receptor and neu receptor and neu receptor expression in proliferative glomerulonephritis. Pathology, 25(4), 327-32.

An immunohistological study of epidermal growth factor receptor and neu receptor and neu receptor expression in proliferative glomerulonephritis. / Roy-Chaudhury, P; Jones, M C; MacLeod, A M; Haites, N E; Simpson, J G; Power, D A.

In: Pathology, Vol. 25, No. 4, 01.10.1993, p. 327-32.

Research output: Contribution to journalArticle

Roy-Chaudhury, P, Jones, MC, MacLeod, AM, Haites, NE, Simpson, JG & Power, DA 1993, 'An immunohistological study of epidermal growth factor receptor and neu receptor and neu receptor expression in proliferative glomerulonephritis', Pathology, vol. 25, no. 4, pp. 327-32.
Roy-Chaudhury, P ; Jones, M C ; MacLeod, A M ; Haites, N E ; Simpson, J G ; Power, D A. / An immunohistological study of epidermal growth factor receptor and neu receptor and neu receptor expression in proliferative glomerulonephritis. In: Pathology. 1993 ; Vol. 25, No. 4. pp. 327-32.
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AB - Many forms of glomerulonephritis including IgA nephropathy are characterized by mesangial cellular proliferation. Since epidermal growth factor is a potent mitogen for cultured human mesangial cells, we have attempted to localize and quantify the expression of its receptor in normal and abnormal renal biopsies using immunohistochemistry. Using a particular antibody (Amersham, clone EGFR1), the epidermal growth factor receptor (EGF-R) was shown to be predominantly localized in the mesangium of the glomerulus. Visual estimates of intensity of staining suggested that expression of this receptor may be increased in some IgA disease patients with mesangial proliferative glomerular lesions. The neu receptor which has a 50% homology with EGF-R was, however, absent from the glomerulus and cultured mesangial cells did not express detectable levels. Expression of EGF-R by cultured mesangial cells, as assessed by immunostaining, was weak and it was not possible to induce detectable upregulation using different cytokines. The factors leading to increased expression of EGF-R in glomerulonephritis, therefore, remain unknown. Our findings suggest that signalling via EGF-R may play a role in the pathogenesis of proliferative glomerulonephritis. Despite its homology with EGF-R, the neu receptor is unlikely to have similar importance.

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