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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2005-1-13
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pubmed:abstractText |
To elucidate the contribution of signal transducer and activator of transcription (STAT) 6 to the pathophysiology of chronic renal injury, STAT6-/- mice were subjected to unilateral ureteral ligation together with wild-type control mice. STAT6-/- kidneys had more apoptotic cells and a greater influx of F4/80-positive cells than wild-type kidneys following ureteral obstruction. There was a much larger alpha-smooth muscle actin-positive area in STAT6-/- kidneys than in wild-type kidneys after ureteral ligation. However, renal fibrosis, as quantified by Masson-Trichrome staining, was not significantly exaggerated in STAT6-/- kidneys compared with wild-type kidneys. The accumulation of collagen I was significantly less in STAT6-/- kidneys than in wild-type kidneys. These observations indicate that the STAT6 signal transduction pathway exerts a protective role on renal cell apoptosis in chronic obstructive uropathy. Our findings also suggest that the STAT6 pathway may have a promotive effect on renal fibrosis by activating collagen synthesis following ureteral obstruction.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1107-3756
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pubmed:author |
pubmed-author:AkiraShizuoS,
pubmed-author:BaiTaoT,
pubmed-author:GodaMikakoM,
pubmed-author:IchinoseMasakazuM,
pubmed-author:KimuraAkihikoA,
pubmed-author:KishinoMasanoriM,
pubmed-author:LiangXiang-MingXM,
pubmed-author:MaedaMasanobuM,
pubmed-author:Owada-MakabeKyokoK,
pubmed-author:TakedaKiyoshiK,
pubmed-author:TanakaTetsujiT,
pubmed-author:TsubotaYujiY,
pubmed-author:UeyamaTakashiT,
pubmed-author:YukawaKazunoriK
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pubmed:issnType |
Print
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pubmed:volume |
15
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
225-30
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pubmed:dateRevised |
2005-11-17
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pubmed:meshHeading |
pubmed-meshheading:15647835-Actins,
pubmed-meshheading:15647835-Animals,
pubmed-meshheading:15647835-Apoptosis,
pubmed-meshheading:15647835-Collagen,
pubmed-meshheading:15647835-Coloring Agents,
pubmed-meshheading:15647835-Fibrosis,
pubmed-meshheading:15647835-Genotype,
pubmed-meshheading:15647835-Immunohistochemistry,
pubmed-meshheading:15647835-In Situ Nick-End Labeling,
pubmed-meshheading:15647835-Kidney,
pubmed-meshheading:15647835-Kidney Diseases,
pubmed-meshheading:15647835-Macrophages,
pubmed-meshheading:15647835-Mice,
pubmed-meshheading:15647835-Mice, Inbred C57BL,
pubmed-meshheading:15647835-Mice, Knockout,
pubmed-meshheading:15647835-Mice, Transgenic,
pubmed-meshheading:15647835-Muscle, Smooth,
pubmed-meshheading:15647835-Nephritis, Interstitial,
pubmed-meshheading:15647835-STAT6 Transcription Factor,
pubmed-meshheading:15647835-Signal Transduction,
pubmed-meshheading:15647835-Time Factors,
pubmed-meshheading:15647835-Trans-Activators,
pubmed-meshheading:15647835-Ureter,
pubmed-meshheading:15647835-Ureteral Obstruction
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pubmed:year |
2005
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pubmed:articleTitle |
STAT6 deficiency inhibits tubulointerstitial fibrosis in obstructive nephropathy.
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pubmed:affiliation |
Department of Physiology, Wakayama Medical University, Wakayama 641-8509, Japan. kazu59@wakayama-med.ac.jp
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pubmed:publicationType |
Journal Article
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