| Budget Amount *help |
¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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| Outline of Final Research Achievements |
We demonstrated that myeloid Fli1 deficiency impaired vasculogenesis due to aberrant vascular mural cells derived from Fli deficient myeloid cells. Vascular instability caused by insufficient function of vascular mural cells are called "pericyte loss".Consistently, pericyte loss caused by impaired vasculogenesis due to myeloid Fli1 deficiency induced characteristic vasculopathy such as proliferative vasculopathy and destructive vasculopathy in the skin vessels. These results suggest that transcription factor Fli1 play important roles as a genetic factor in the pathogenesis of characteristic vasculopathy in systemic sclerosis. In addition, these vasculopathy induced by myeloid Fli1 deficiency was partially reversed by dual endothelin receptor blocker bosentan.
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