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
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