Glomerular and tubular induction of the transcription factor c-Jun in human renal disease
Autor: | Robbert J. Kok, Jai Prakash, Gerarda Navis, van Harry Goor, M. C. van den Heuvel, Wynand B. W. H. Melenhorst, de Martin Borst |
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Přispěvatelé: | Faculteit Medische Wetenschappen/UMCG, Nanomedicine & Drug Targeting, Groningen Kidney Center (GKC), Groningen Institute for Organ Transplantation (GIOT) |
Rok vydání: | 2007 |
Předmět: |
Male
Proto-Oncogene Proteins c-jun TERMINAL KINASE Kidney Glomerulus NF-KAPPA-B Kidney Immunoenzyme Techniques Transforming Growth Factor beta Membranoproliferative glomerulonephritis Minimal change disease Hepatitis A Virus Cellular Receptor 1 Cells Cultured Chemokine CCL2 GENE-EXPRESSION Aged 80 and over Membrane Glycoproteins biology c-Jun N-terminal kinase (JNK) c-jun activator protein-1 (AP-1) MONOCYTE CHEMOATTRACTANT PROTEIN-1 Glomerulonephritis Middle Aged Kidney Tubules AP-1 ACTIVATION medicine.anatomical_structure kidney human renal disease Receptors Virus Female Kidney Diseases Glomerular Filtration Rate Adult medicine.medical_specialty Collagen Type I Pathology and Forensic Medicine Nephropathy HUMAN ENDOTHELIAL-CELLS GLOMERULONEPHRITIS MESANGIAL CELLS Internal medicine INJURY medicine Humans biopsy Human renal disease RESPONSE ELEMENTS Aged Cell Proliferation Activating Transcription Factor 2 business.industry Macrophages c-Jun Transforming growth factor beta medicine.disease Collagen Type I alpha 1 Chain Endocrinology biology.protein business Kidney disease |
Zdroj: | JOURNAL OF PATHOLOGY, 213(2), 219-228. Wiley Journal of pathology, 213(2), 219-228. Wiley |
ISSN: | 1096-9896 0022-3417 |
Popis: | The transcription factor c-Jun regulates the expression of genes involved in proliferation and inflammation in many cell types but its role in human renal disease is largely unclear. In the current study we investigated whether c-Jun activation is associated with human renal disease and if c-Jun activation regulates pro-inflammatory and pro-fibrotic genes in renal cells. Activation of c-Jun was quantified by scoring renal expression of phosphorylated c-Jun (pc-Jun) in control human renal tissue and in biopsies from patients with various renal diseases (diabetic nephropathy, focal glomerulosclerosis, hypertension, IgA nephropathy, membranous glomerulopathy, minimal change disease, membranoproliferative glomerulonephritis, systemic lupus erythematosus, acute rejection, and Wegener's granulomaiosis); this was correlated with parameters of renal damage. Furthermore, we studied the functional role of c-Jun activation in human tubular epithelial cells (HK-2) stimulated with TGF-ss. Activated c-Jun was present in nuclei of glomerular and tubular cells in all human renal diseases, but only sporadically in controls. Across the diseases, the extent of pc-Jun expression correlated with the degree of focal glomerulosclerosis, interstitial fibrosis, cell proliferation, kidney injury molecule-1 (Kim-1) expression, macrophage accumulation, and impairment of renal function. In HK-2 cells,'TGF-ss induced c-Jun activation after 1 h (+40%, p |
Databáze: | OpenAIRE |
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