구성원

구성원

정일엽

Dongtak Jeong 정동탁 교수

  • DepartmentDepartmentProf. Dept. of Medicinal and Life Sciences, College of Science and Convergence Technology / Professor
  • E-mailE-mailcooljdt@hanynag.ac.kr
  • Office PhoneOffice Phone031-400-5515
  • HomepageHomepagehttps://cooljdt.wixsite.com/mmllab
  • 학과/직책학과/직책과학기술융합대학 의약생명과학과 / 교수
  • 이메일이메일cooljdt@hanynag.ac.kr
  • 전화번호전화번호031-400-5515
  • 홈페이지홈페이지https://cooljdt.wixsite.com/mmllab
Research Keywords
연구키워드
  • #cardiovascular disease #Cardiac hypertrophy #cellular fibrosis #miRNA #Gene Theapy #AAV #Calcium signal transduction #Cellular Senescence #Pulmonary Arterial hypertension #modRNA
  • #심혈관 질환 #심근비대증 #세포 섬유화 #miRNA #유전자 치료 #AAV #칼슘 신호전달 #세포 노화 #폐동맥 고혈압 #modRNA
Research Objectives
연구목표
  • Gene therapy on cardiovascular diseases
  • Cardiac gene therapy using miRNA tough decoy inhibitor in heart failure
  • CCN5 gene delivery to regulate cardiac hypertrophy and arrhythmias
  • Study on the inflammatory mechanism to regulate cardiac fibrosis
  • The Effect of PLN peptide decoy on pulmonary arterial hypertension model
  • Discovery of therapeutic candidates to treat senescence-induced cardiac dysfunction
  • 유전자 치료법을 이용한 다양한 심혈관질환 치료
  • miRNA-21/ miRNA-25 miRNA 터프 데코이 (TuD)를 이용한 심장병 치료
  • CCN5 및 Cytl1을 사용하여 심장섬유증 및 심방부정맥 치료
  • 심장 섬유증을 조절하는 NLRP3 염증 신호 경로 조절 기작 규명
  • 폐동맥 고혈압을 치료하기 위한 PLN peptide decoy 효능 및 기전 규명
  • 세포 노화에 의한 심장병 기전 규명 및 치료후보물질 개발
Brief Research Experience
주요경력
  • Professor, Hanyang University ERICA Campus (2022-present)
  • Associate Professor, Hanyang University ERICA Campus (2020-2022)
  • Assistant Professor, Cardiovascular Research center, Icahn School of Medicine at Mount Sinai, NY, USA
  • Instructor, Cardiovascular Research center, Icahn School of Medicine at Mount Sinai, NY, USA
  • SCI Publications: 51papers, 3 Book chapters, 4 patents
  • Associate Editor, Frontiers in Cardiovascular Medicine (2021-present)
  • Guest Editor, Pharmaceuticals (2020-present)
  • Guest Editor, International Journal of Molecular Science(2020-present)
  • 한양대학교 과학기술대학 분자생명과학과 교수 (2022-현재)
  • 한양대학교 과학기술대학 분자생명과학과 부교수 (2020-2022)
  • 미국 뉴욕 마운트 시나이 의과대학 심혈관 연구센터 조교수 (2018-2020)
  • 미국 뉴욕 마운트 시나이 의과대학 심혈관 연구센터 전임강사 (2013-2018)
  • SCI 논문 51편 게재. 저서(chapter) 3권, 특허 4건
  • h-index: 29, 3400회 (Google scholar 기준)
  • 부편집장, Frontiers in Cardiovascular Medicine (2021-현재)
  • 객원편집장, Pharmaceuticals (2020-현재)
  • 객원편집장, International Journal of Molecular Science(2020-현재)
Research Areas
연구분야
  • Study on the role of miR-25 in cardiac dysfunction and fibrosis
  • Discovery of therapeutic candidates to treat senescence-induced cardiac dysfunction
  • CCN5 gene delivery to regulate cardiac hypertrophy and arrhythmias
  • Discovery of therapeutic candidates using DMD patient-derived iPS cells
  • miR-25의 조절을 통한 심근증 및 심장 섬유화의 기전확립 / 치료기술 개발
  • 세포 노화에 의한 심장병 기전 규명 및 치료후보물질 개발
  • CCN5 및 Cytl1을 사용하여 심장섬유증 및 심방부정맥 치료
  • 환자 유래 iPS 세포이용한 치료 후보 유전자 발굴
Thesis
논문
  • Wahlquist C, Jeong D, Rojas-Muñoz A, Kho C, Lee A, Mitsuyama S, van Mil A, Park WJ, Sluijter JP, Doevendans PA, Hajjar RJ, Mercola M. (2014). Inhibition of miR-25 improves cardiac contractility in the failing heart. Nature. 508(7497):531-5.
  • Lee A, Jeong D, Mitsuyama S, Oh JG, Liang L, Ikeda Y, Sadoshima J, Hajjar R, Kho C. (2014). The Role of SUMO-1 in Cardiac Oxidative Stress and Hypertrophy. Antioxid Redox Signal. 21(14):1986-2001.
  • Jeong D, PhD, Lee M, Li Y, Kho C, et al. (2016) The Matricellular Protein CCN5 Reverses Established Cardiac Fibrosis. J Am Coll Cardiol. 67(13):1556-1568.
  • Jeong D, Yoo J, Lee P, Kepreotis SV, Lee A, Wahlquist C, Brown BD, Kho C, Mercola M, Hajjar RJ. (2018) miR-25 Tough Decoy Enhances Cardiac Function in Heart Failure. Mol Ther. 26(3):718-729.
  • Oh JG, Jang SP, Yoo J, Lee MA, Lee SH, Lim T, Jeong E, Kho C, Kook H, Hajjar RJ, Park WJ, Jeong D. (2019) Role of the PRC2-Six1-miR-25 signaling axis in heart failure. J Mol Cell Cardiol. 129:58-68.
  • Katz MG, Fargnoli AS, Hajjar RJ, Jeong D. (2019)MicroRNA-25 upregulation protects spinal cords, yet is bad for the heart: The dark side of noncoding RNAs. J Thorac Cardiovasc Surg. 158(3):e87-e88.
  • Gorski PA*, Jang SP*, Jeong D*, Lee A, Lee P, Oh JG, Chepurko V, Yang DK, Kwak TH, Eom SH, Park ZY, Yoo YJ, Kim DH, Kook H, Sunagawa Y, Morimoto T, Hasegawa K, Sadoshima J, Hajjar RJ, Park WJ, Kho C. (2019) Role of SIRT1 in Modulating Acetylation of the Sarco-Endoplasmic Reticulum Ca2+-ATPase in Heart Failure. Circ Res. 124(9):e63-e80.
  • Oh JG, Lee P, Gordon RE, Sahoo S, Kho C, Jeong D. (2020) Analysis of extracellular vesicle miRNA profiles in heart failure. J Cell Mol Med. 24(13):7214-7227.
  • Lee M, Raad N, Song MH, Yoo J, Lee M, Jang SP, Kwak TH, Kook H, Choi E, Cha T, Hajjar RJ, Jeong D, Park WJ. (2020). The matricellular protein CCN5 prevents adverse atrial structural and electrical remodeling. J Cell Mol Med. 24(20):11768-11778.
  • Song MH, Yoo J, Oh JG, Kook H, Park WJ, Jeong D. (2022) Matricellular Protein CCN5 Gene Transfer Ameliorates Cardiac and Skeletal Dysfunction in mdx/utrn (+/-) Haploinsufficient Mice by Reducing Fibrosis and Upregulating Utrophin expression. Front Cardiovasc Med. 9:763544.
Research Topics
연구내용
  • Cardiac gene therapy to treat cardiovascular diseases

    Restoration of cardiac contractility through the regulation of miRNA-25 expression

    Alleviation of cardiac fibrosis using CCN5 gene delivery

    Regulation of tissue fibrosis through the treatment of inhibitor ofthe Cytl1 gene expression

    Discovery of therapeutic candidates to treat senescence-induced cardiac dysfunction

  • Discovery of therapeutic candidates to treat DMD induced-cardiomyopathy

    Inhibition of cellular senescence using CCN5 gene therapy

    Enhancement of immune system by CCN5 treatment

    Therapeutic efficacy and efficiency of mRNA-mediated gene delivery in cardiovascular diseases

    Novel gene delivery methods using gold / lipid nanoparticles

    Modification of mosaic AAV viruses to evade host immune response to enhance the efficiency of gene delivery

    Pre-clinical application of CCN5 in patient-derived iPS cells

    Application of discovered genes as therapeutic candidates to various cardiovascular disease models