Document Detail


Activation of signal transducer and activator of transcription 3 correlates with cell proliferation and renal injury in human glomerulonephritis.
MedLine Citation:
PMID:  18556750     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Signal transducer and activator of transcription (STAT) 3 plays an important role in the regulation of cell proliferation. However, the mechanism of STAT3 activation in human glomerulonephritis is unclear. METHODS: STAT3 activation was determined using immunohistochemistry for phosphorylated STAT3 (p-STAT3) in normal human kidney and various types of glomerulonephritis. We also identified the cell exhibiting activated p-STAT3 expression in human glomerulonephritis and correlated STAT3 activation with renal function and histologic injury. RESULTS: p-STAT3 staining was identified in glomeruli and some tubules in normal human kidney. p-STAT3 positive glomerular cells were significantly increased in lupus nephritis, IgA nephropathy and vasculitis compared with normal kidney. p-STAT3 positive tubulointerstitial cells were significantly increased in IgA nephropathy and vasculitis compared with normal kidney. Glomerular and tubulointerstitial p-STAT3 staining was significantly decreased after steroid therapy. There was a significant correlation between the number of p-STAT3 positive cells and the number of PCNA positive glomerular and tubulointerstitial cells in all cases of glomerulonephritis. Furthermore, renal function inversely correlated with the number of p-STAT3 positive glomerular and tubulointerstitial cells in all cases of glomerulonephritis. CONCLUSIONS: The present study has identified STAT3 activation in normal human kidney and a marked increase in STAT3 activation in many forms of glomerulonephritis. The correlation of STAT3 activation with clinical and histologic parameters suggests that this pathway plays an important role in the pathogenesis of kidney disease. Furthermore, localization of STAT3 activation to individual cell types suggests that this pathway may play a pivotal role in promoting renal inflammation and fibrosis.
Authors:
Tetsuji Arakawa; Takao Masaki; Takayuki Hirai; Shigehiro Doi; Masatoshi Kuratsune; Koji Arihiro; Nobuoki Kohno; Noriaki Yorioka
Publication Detail:
Type:  Journal Article     Date:  2008-06-13
Journal Detail:
Title:  Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association     Volume:  23     ISSN:  1460-2385     ISO Abbreviation:  Nephrol. Dial. Transplant.     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-10-16     Completed Date:  2009-03-02     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8706402     Medline TA:  Nephrol Dial Transplant     Country:  England    
Other Details:
Languages:  eng     Pagination:  3418-26     Citation Subset:  IM    
Affiliation:
Department of Molecular and Internal Medicine, Graduate School of Biomedical Sciences, Hiroshima University, Minami-ku, Hiroshima City 734-8551, Japan.
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MeSH Terms
Descriptor/Qualifier:
Adolescent
Adult
Aged
Aged, 80 and over
Biopsy
Case-Control Studies
Cell Proliferation*
Female
Glomerulonephritis / metabolism*,  pathology
Glomerulonephritis, IGA / metabolism,  pathology
Humans
Kidney / metabolism*,  pathology*
Lupus Nephritis / metabolism,  pathology
Male
Middle Aged
STAT3 Transcription Factor / metabolism*
Signal Transduction / physiology
Vasculitis / metabolism,  pathology
Young Adult
Chemical
Reg. No./Substance:
0/STAT3 Transcription Factor; 0/STAT3 protein, human

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