| Project/Area Number |
18590385
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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 |
Experimental pathology
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| Research Institution | Toho University |
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Principal Investigator |
AKASAKA Yoshikiyo Toho University, Faculty of Medicine, Associate Professor (60202511)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIKAWA Yukio Toho University, Faculty of Medicine, Associate Professor (30276894)
ONO Ichiro Sappro Medical University, School of Medicine, Associate Professor (20125298)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,880,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥480,000)
Fiscal Year 2007: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2006: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Wound healine / Mvofibroblast / Apoptosis / hFGF / TGF-β1 / α-SMA |
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| Research Abstract |
To examine the effect of bFGF on inhibition of a-SMA expression in dermal fibroblasts, we have established two dermal myofibroblastic lines positive for a-SMA RMFL cell lines) and one fibroblastic line negative for a-SMA (RF cell line) as a model of fibroblast differentiation. In contrast to the increased expression of a-SMA in the RMF and RMFL cell lines with or without TGF-β1 treatment, bFGF induced a decrease of a-SMA expression in the myofibroblastic lines and the reduced expression patterns of a-SMA were different between them, as demonstrated by Western blot and RT-PCR analyses. Along with the inhibition of a-SMA expression in the RMF and RMFL cell lines by bFGF, different activated expression of ERK1/2 were also detected in them, suggesting the involvement of ERK1/2 activation in downregulation of a-SMA expression in the myofibroblastic lines. Furthermore, in vivo study demonstrated that bFGF administration decreased the area positive for a-SMA expression in the open wounds in the later phase of healing. These results together indicate that bFGF is a potent stimulator of downregulation of α-SMA expression in dermal myofibroblasts, suggesting the possible role of bFGF in the modulation toward fibroblasts from myofibroblasts in vivo.
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