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Travel Award
As Editor-in-Chief of the Journal of Cardiovascular Development and Disease (JCDD), I am pleased to announce that the winner of the 2017 JCDD Travel Award, is Dr. Jae Gyun Oh, a Postdoctoral researcher in Prof. Roger J. Hajjar’s laboratory at Icahn School of Medicine at Mt Sinai, NY, USA, who will receive 800 Swiss Francs towards travel expenses to attend 2017 Keystone Symposia to be held in Keystone, CO, USA.
Dr. Oh’s current research focuses on the role of miR-146a as a SUMO1 targeting microRNA (miR). SUMO1 has been shown to be a critical player in heart failure (HF) pathophysiology. The expression of miR-146a shows an inverse correlation with SUMO1. In his project, Dr. Oh investigated which cell types contribute to miR-146a expression. He analyzed isolated myocyte and non-myocyte fractions from normal and failing hearts and determined that during HF, upregulation of miR-146a and downregulation of SUMO1 was confirmed in cardiomyocytes, but that the amount of pri-mir-146a indicating transcription of miR-146a was increased only in nonmyocytes.
He tested the hypothesis that cell-to-cell transfer of mature miR-146a can explain the increase in miR-146a in cardiomyocytes and found that miR-146a is mainly secreted from fibroblasts via exosomes and that these fibroblast exosomes are taken up by cardiomyocytes. The major conclusion of Dr. Oh’s research presented in his abstract for this meeting is that fibroblasts are a major source of miR-146a during HF, and exosome-mediated miR-146a transfer is a critical mechanism of cardiomyocyte function.
Dr. Oh’s current research focuses on the role of miR-146a as a SUMO1 targeting microRNA (miR). SUMO1 has been shown to be a critical player in heart failure (HF) pathophysiology. The expression of miR-146a shows an inverse correlation with SUMO1. In his project, Dr. Oh investigated which cell types contribute to miR-146a expression. He analyzed isolated myocyte and non-myocyte fractions from normal and failing hearts and determined that during HF, upregulation of miR-146a and downregulation of SUMO1 was confirmed in cardiomyocytes, but that the amount of pri-mir-146a indicating transcription of miR-146a was increased only in nonmyocytes.
He tested the hypothesis that cell-to-cell transfer of mature miR-146a can explain the increase in miR-146a in cardiomyocytes and found that miR-146a is mainly secreted from fibroblasts via exosomes and that these fibroblast exosomes are taken up by cardiomyocytes. The major conclusion of Dr. Oh’s research presented in his abstract for this meeting is that fibroblasts are a major source of miR-146a during HF, and exosome-mediated miR-146a transfer is a critical mechanism of cardiomyocyte function.
Journal of Cardiovascular Development and Disease Travel Award
Winners announced
Past Winners
Winner
- JSJunichi SaitoJunichi SaitoYale University, USA
Hannah TarolliHannah TarolliMedical University of South Carolina, USA
Award Committee
Thomas BrandThomas BrandImperial College London, UKChairman
Maria Grazia AndreassiMaria Grazia AndreassiCNR Institute of Clinical Physiology, Italy
Paolo Emilio PudduPaolo Emilio PudduSapienza University of Rome, Italy
Óscar Lorenzo GonzálezÓscar Lorenzo GonzálezUniversidad Autonoma de Madrid, Spain

