| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Outline of Final Research Achievements |
Aryl hydrocarbon receptor (AhR) plays crucial roles in the protection against xenobiotics exposure. Recent report showed that 6-formylindolo[3,2-b]carbazole (FICZ) was one of the endogenous AhR ligands. We previously revealed that FICZ promoted cutaneous wound healing in various mouse models, including db/db mice, which exhibited delayed wound healing. However, the molecular mechanism underlying the wound healing acceleration by FICZ remains unclear. Here, we first demonstrated that FICZ promoted the migration of human keratinocytes via an increased MEK and ERK phosphorylation under scratch condition. Cell migration induced by FICZ was suppressed by MEK/ERK inhibitors, but not EGFR inhibitor. In addition, FICZ accelerated wound closure irrespective of AhR expression. Our findings indicate that FICZ has potential as an enhancer of cell migration via activation of MEK/ERK pathway in an AhR-independent manner, and might be beneficial for wound healing.
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