Molecular mechanistic study for epigenome-switch on endothelial cell activation

2015 Fiscal Year Final Research Report

• Project/Area Number: 26640069
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Tumor biology
• Research Institution: Kumamoto University (2015); The University of Tokyo (2014)
• Principal Investigator: MINAMI Takashi 熊本大学, 生命資源研究支援センター, 教授 (00345141)
• Co-Investigator(Renkei-kenkyūsha): KANKI Yasuharu 東京大学, アイソトープ総合センター, 助教 (00534869)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: エピゲノム制御 / 血管内皮細胞 / VEGF / ChIP-seq / NFAT / 転写制御 / 血管新生 / ヒストンプロファイル

Outline of Final Research Achievements

Angiogenesis based on the inner endothelial proper proliferation via growth factor or cytokines such as VEGF. We comprehensively surveyed VEGF signaling by using HUVEC, resulted the findings of dynamic epigenome alteration following the NFAT nuclear localization. ChIP-seq experiments by using the NFATc1 antibody resulted that SDF-1 receptor; CXCR7, and RhoA modulator, RND1 were newly picked up for the NFAT downstream angiogenesis regulator. Moreover, our epigenome profiling data indicated that bivalent histone marks which means double positive for transcriptional active; H3K4me3 and brake; H3K27me3, were enriched on the regulatory regions of acute angiogenic transcription factor family. Our ChIP-re chip experiment successfully indicated that such a bivalent histone modification was occurred in single cell level and not reflect the cell mixture condition from either only H3K4me3 positive cells and H3L27me3 positive cells.

Free Research Field

血管生物学