Multi-tracer molecular imaging for the assessment of pathophysiology of ventricular remodeling after myocardial infarction

2016 Fiscal Year Final Research Report

• Project/Area Number: 26461847
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Radiation science
• Research Institution: Kanazawa University
• Principal Investigator: Taki Junichi 金沢大学, 附属病院, 講師 (10251927)
• Research Collaborator: WAKABASHI Hiroshi 金沢大学, 附属病院, 助教 (60622818) ; INAKI Anri 金沢大学, 医学系, 協力研究員 (40645131)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: myocardial ischemia / remodeling / tenascin C / angiogenesis / RGD / apoptosis / annexin V

Outline of Final Research Achievements

Tenascin-C expression after myocardial ischemia and reperfusion was investigated using I-125-anti-tneascin-c-antibody (TNC). Autoradiography showed that the uptake peaked 3 days after reperfusion, followed by gradual reduction. Postconditioning at reperfusion suppressed TNC uptake at day 3 and thereafter and attenuated the left ventricular remodeling at 2 months later, suggesting that suppression of tenascin-C expression related to the attenuation of ventricular remodeling.
αvβ3 integrin is expressed both by macrophages and angiogenic endothelial cells. We investigated whether I-125-RGD, which showed high affinity and selectivity for αvβ3, reflects inflammatory process or angiogenesis after myocardial infarction. I-125 RGD accumulated in the infarcted area, and its uptake corresponded closely to micro vessel formation rather than macrophage infiltrations until 2 months after infarction. RGD imaging may be useful for the evaluation of angiogenesis after myocardial infarction.

Free Research Field

核医学