The mechanism of actin metabolism abnormality in a hereditary small vessel disease and development of novel treatment

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K18387
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Nerve anatomy/Neuropathology
• Research Institution: National Cardiovascular Center Research Institute
• Principal Investigator: Yamamoto Yumi 国立研究開発法人国立循環器病研究センター, 研究所, 流動研究員 (10614927)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: CADASIL / 脳血管障害 / 脳梗塞 / 壁細胞

Outline of Final Research Achievements

We have established a technique to differentiate iPS cells into mural cells (iPSMCs). We differentiated iPS cells from patients with hereditary small vessel disease, CADASIL into iPSMCs and compared their properties with controls. The CADASIL iPSMCs showed increased expression of PDGFRbeta and promoted migration, which were suggested to be closely involved in CADASIL pathogenesis. The knockdown of mutant NOTCH3 and/or PDGFRbeta significantly suppressed the promoted migration in CADASIL iPSMCs. These genes may be ideal targets for novel treatment of CADASIL.

Free Research Field

脳血管障害