Study of Cardioprotective Signal through STAT3/Pim Kinase

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08232
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General pharmacology
• Research Institution: Osaka University
• Principal Investigator: Makiko Maeda 大阪大学, 薬学研究科, 准教授 (70461168)
• Co-Investigator(Kenkyū-buntansha): 藤尾 慈 大阪大学, 薬学研究科, 教授 (20359839)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 虚血性心疾患 / 心筋保護シグナル

Outline of Final Research Achievements

Cardioprotective effect is known to be very important to maintain cardiac homeostasis. Silvestrol, a naturally occurring member of the flavagline family of compounds, inhibits cap-dependent translation by targeting eIF4A, and it is known to decrease the expression of cancer genes. It is also reported that eIF4 family has cell protective effects and eIF4B, exhibits various kinds of biological functions. In cancer cells, eIF4B is activated by Pim-1 kinase. However, pathophysiological roles of Pim-1/eIF4B remain to be elucidated in cardiomyocytes.
In this study, we focused on N-cadherin, which is involved in cell-cell adhesion, and proved whether STAT3/Pim-1/eIF4B/ N-cadherin signaling pathway in cardiomyocytes could work for cardioprotective effects.
The proposal from the results of this study may support the possibility of cardioprotective effect by cell-cell adhesion control through STAT3/Pim-1 signaling pathway.

Free Research Field

医療薬学