| Project/Area Number |
11671042
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
KATOH Tetsuo Fukushima Medical University, Department of Medicine, Lecturer, 医学部, 講師 (70194834)
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| Co-Investigator(Kenkyū-buntansha) |
ASAHI Koichi Fukushima Medical University, Department of Medicine, Assistant Professor, 医学部, 助手 (60274966)
ASANO Kenichiro Fukushima Medical University, Department of Medicine, Assistant Professor, 医学部, 助手 (20315659)
栗城 実 福島県立医科大学, 医学部, 助手 (00295411)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1999: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | TGF-β / Smad / Mesangial cell / collagen / Fibronectine / TGF-β / Collagen / コラーゲン |
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| Research Abstract |
Mechanical stretch, an in vitro model of glomerular hypertension, increases extracellular matrix (ECM) production via transforming growth factor-β (TGF-β) signaling in cultured rat mesangial cells (MCs). Recently, Smads have been identified as intracellular molecules of TGF-β superfamily. Especially, Smad6 and Smad7 are termed as inhibitory Smads (l-Smads), cause Smad6 and Smad7 have antagonistic a roles through TGF-β signaling. In cultured cells under static condition, exogenous TGF-β 1 up-regulates gene expression of inhibitory Smads gene expression and thereby constituting negative feedback loops in the action of TQF-β. Although various studies of l-Smads were performed under static culture condition, we studied the gene expression of inhibitory Smads in cultured rat mesangial cells under mechanical stretch. Rat MCs were cultured on collagen type I coated plates and stimulated by mechanical stretch or exogenous TGF-β1. Smad6 and Smad7 gene expression were evaluated by northern blot analysis. Relative amount of phospho-Smad2/3 after TGF-β1 treatment was compared with between pre-stretch group and non-stretch group by western blot using anti-phospho-Smad2/3 antibody. In static condition, l-Smads mRNA were significantly increased by exogenous TGF-β1 after 1.5-3 hours and returned to the control levels. Under mechanical stretch (15-20% elongation for 3 hours), although the amount of TGF-β1
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