Project/Area Number |
26250033
|
Research Category |
Grant-in-Aid for Scientific Research (A)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Tumor therapeutics
|
Research Institution | Osaka University |
Principal Investigator |
MEKADA EISUKE 大阪大学, 微生物病研究所, 教授 (20135742)
|
Co-Investigator(Renkei-kenkyūsha) |
IWAMOTO Ryo 大阪大学, 微生物病研究所, 准教授 (10213323)
MIZUSHIMA Hiroto 大阪大学, 微生物病研究所, 助教 (30379094)
NAKAMURA Takashi 大阪大学, 微生物病研究所, 研究員 (00570673)
|
Research Collaborator |
YONEDA Tomoko 大阪大学, 微生物病研究所, 特任技術職員
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥40,300,000 (Direct Cost: ¥31,000,000、Indirect Cost: ¥9,300,000)
Fiscal Year 2016: ¥12,480,000 (Direct Cost: ¥9,600,000、Indirect Cost: ¥2,880,000)
Fiscal Year 2015: ¥12,480,000 (Direct Cost: ¥9,600,000、Indirect Cost: ¥2,880,000)
Fiscal Year 2014: ¥15,340,000 (Direct Cost: ¥11,800,000、Indirect Cost: ¥3,540,000)
|
Keywords | EGFR / HB-EGF / ErbB4 / 増殖抑制 / EGF受容体 / 細胞増殖因子 / マイコプラズマ |
Outline of Final Research Achievements |
HB-EGF plays an indispensable role in suppression of cell proliferation in mouse valvulogenesis. However, ligands of the EGF receptor (EGFR/ErbB1), including HB-EGF, are generally considered as growth-promoting factors, as shown in cancers. We investigated the role of ErbB receptors in valvulogenesis in vivo using ErbB1- and ErbB4-deficient mice, and an ex vivo model of endocardial cushion explants. We found that HB-EGF suppresses valve mesenchymal cell proliferation through a heterodimer of ErbB1 and ErbB4, and an ErbB1 ligand(s) promotes cell proliferation through a homodimer of ErbB1. Our study demonstrates that opposing signals generated by different ErbB dimer combinations function in the same cardiac cushion mesenchymal cells for proper cardiac valve formation.
|