The role of interleukin-17 in left ventricular remodeling of acute myocardial infarction

• Project/Area Number: 26861538
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Emergency medicine
• Research Institution: Kurume University
• Principal Investigator: SASAKI Tomoko 久留米大学, 医学部, 助教 (30597430)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Project Status: Completed (Fiscal Year 2017)
• Budget Amount: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000); Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000); Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
• Keywords: サイトカイン / 急性心筋梗塞 / 炎症 / IL17 / 心筋梗塞 / 分子生物学 / リモデリング

Outline of Final Research Achievements

Interleukin-17 (IL-17) is a key cytokine produced by activated lymphocytes, which plays pathogenic roles in the development of inflammatory diseases. Cardiac rupture after myocardial infarction(AMI) is a fatal complication, however, little is known about the role of inflammatory process in the onset of cardiac rupture. We induced permanent ligation of the left anterior descending coronary artery in IL17 knockout mice (IL17-KO) and wild-type (WT) mice. Approximately 30% of WT mice died with cardiac rupture after AMI. In contrast, none of the IL17-KO mice had cardiac rupture. Immunostaining showed that neutrophils and macrophages infiltration in the hearts were less in IL17-KO mice than WT mice. Real-time PCR revealed that the expressions of inflammatory molecules were less in IL17-KO mice than those in WT mice. These results suggest that cardiac rupture after AMI is prevented in IL17-KO mice by inhibiting leukocytes infiltration and inflammatory genes expression.

Research Products

• [Journal Article] Renal nerve-mediated erythropoietin release confers cardioprotection during remote ischemic preconditioning. (2015)
  • Author(s): Oba T, Yasukawa H, Nagata T, Kyogoku S, Minami T, Nishihara M, Ohshima H, Mawatari K, Nohara S, Takahashi J, Sugi Y, Igata S, Iwamoto Y, Kai H, Matsuoka H, Takano M, Aoki H, Fukumoto Y, Imaizumi T.
  • Journal Title: Circulation Journal Volume: 印刷中
  • NAID: 130005083944
  • Peer Reviewed
• [Journal Article] Cardiac-Specific SOCS3 Deletion Prevents In Vivo Myocardial Ischemia Reperfusion Injury through Sustained Activation of Cardioprotective Signaling Molecules (2015)
  • Author(s): Nagata T, Yasukawa H, Kyogoku S, Oba T, Takahashi J, Nohara S, Minami T, Mawatari K, Sugi Y, Shimozono K, Pradervand S, Hoshijima M, Aoki H, Fukumoto Y, Imaizumi T
  • Journal Title: PLOS ONE Volume: 印刷中
  • Peer Reviewed
• [Journal Article] Disturbance of cardiac gene expression and cardiomyocyte structure predisposes Mecp2-null mice to arrhythmias. (2015)
  • Author(s): Hara M, Takahashi T, Mistumasu C, Igata S, Takano M, Minami T, Yasukawa H, Okayama S, Nakamura K, Okabe Y, Tanaka E, Takemura G, Kosai K, Yamashita Y, Matsuishi T
  • Journal Title: Sci Rep Volume: 印刷中
  • Peer Reviewed
• [Presentation] Interleukin-17 Deletion Prevents Cardiac Rupture after Acute Myocardial Infarction in Mice (2017)
  • Author(s): Tomoko Sasaki, Hideo Yasukawa, Kazutoshi Mawatari, Daisuke Fukui, Takanobu Nagata, Sachiko Kyogoku, Hideki Ohshima, Jinya Takahashi, Shoichiro Nohara, Koutatsu Shimozono, Tatsuhiro Shibata, Yoshihiro Fukumoto
  • Organizer: 第81回日本循環器学会学術集会
  • Place of Presentation: 金沢市教育プラザ此花（石川県金沢市）
  • Year and Date: 2017-03-17