| Budget Amount *help |
¥137,280,000 (Direct Cost: ¥105,600,000、Indirect Cost: ¥31,680,000)
Fiscal Year 2018: ¥26,520,000 (Direct Cost: ¥20,400,000、Indirect Cost: ¥6,120,000)
Fiscal Year 2017: ¥26,520,000 (Direct Cost: ¥20,400,000、Indirect Cost: ¥6,120,000)
Fiscal Year 2016: ¥26,520,000 (Direct Cost: ¥20,400,000、Indirect Cost: ¥6,120,000)
Fiscal Year 2015: ¥26,520,000 (Direct Cost: ¥20,400,000、Indirect Cost: ¥6,120,000)
Fiscal Year 2014: ¥31,200,000 (Direct Cost: ¥24,000,000、Indirect Cost: ¥7,200,000)
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| Outline of Final Research Achievements |
Hair graying and hair thinning are prominent aging phenotypes, yet the underlying mechanisms have been elusive. We previously found that hair follicle stem cells (HFSCs) provide a functional niche for melanocyte stem cells (McSCs). In vivo fate analysis of HFSCs revealed that the DNA damage response in HFSCs causes downregulation of type XVII collagen (COL17A1), a critical molecule for maintenance of HFSCs, to trigger HFSC aging and resultant hair follicle miniaturization. As COL17A1 is not expressed by McSCs but is critical for HFSCs to maintain McSCs, COL17A1 downregulation in HFSCs causes depletion of McSCs through their ectopic differentiation in the niche. The hair follicle aging process can be recapitulated by Col17a1 deficiency and prevented by the forced maintenance of COL17A1 in HFSCs, demonstrating that COL17A1 in HFSCs orchestrates the stem cell-centric aging program of the epithelial mini-organ and indicating potential angles for anti-ageing therapeutic intervention.
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