2016 Fiscal Year Final Research Report
The roles of transcriptional factor Fli1 in the phenotypic changes of SSc myeloid cells
| Project/Area Number |
15H06164
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2015-08-28 – 2017-03-31
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| Keywords | 全身性強皮症 / 血管内皮細胞 / 脈管形成 |
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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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| Free Research Field |
膠原病
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