|Wiesner DL, Specht CA, Lee CK, Smith KD, Mukaremera L, Lee ST, Lee CG, Elias JA, Nielsen JN, Boulware DR, Bohjanen PR, Jenkins MK, Levitz SM, Nielsen K Chitin recognition via chitotriosidase promotes pathologic type-2 helper T cell responses to cryptococcal infection.. PLoS pathogens. 2015; 11 (3) : e1004701.|
|Ahangari, Farida, Sood, Akshay, Ma, Bing, Takyar, Seyedtaghi, Schuyler, Mark, Qualls, Clifford, Dela Cruz, Charles S., Chupp, Geoffrey L., Lee, Chun G., Elias, Jack A. Chitinase 3–like-1 Regulates Both Visceral Fat Accumulation and Asthma-like Th2 Inflammation. Am J Respir Crit Care Med. 2015; 191 (7) : 746-757.|
|Cho, Soo Jung, Weiden, Michael D., Lee, Chun Geun Chitotriosidase in the Pathogenesis of Inflammation, Interstitial Lung Diseases and COPD. Allergy, Asthma & Immunology Research. 2015; 7 (1) : 14.|
|Patel AS, Song JW, Chu SG, Mizumura K, Osorio JC, Shi Y, El-Chemaly S, Lee CG, Rosas IO, Elias JA, Choi AM, Morse D Epithelial cell mitochondrial dysfunction and PINK1 are induced by transforming growth factor-beta1 in pulmonary fibrosis.. PLoS ONE. 2015; 10 (3) : e0121246.|
|Wang J, Liu W, Marion C, Singh R, Andrews N, Lee CG, Elias JA, Dela Cruz CS Interleukin-15 Regulates Retinoic Acid Receptor Beta in the Lung During Cigarette Smoking and Influenza Virus Infection.. American Journal of Respiratory Cell and Molecular Biology. 2015;|
|Ma, B., Herzog, E. L., Lee, C. G., Peng, X., Lee, C.-M., Chen, X., Rockwell, S., Koo, J. S., Kluger, H., Herbst, R. S., Sznol, M., Elias, J. A. Role of chitinase 3-like-1 and semaphorin 7a in pulmonary melanoma metastasis.. Cancer Research. 2015; 75 (3) : 487-496.|
|Kang MJ, Yoon CM, Nam M, Kim DH, Choi JM, Lee CG, Elias JA Role of Chitinase 3-like-1 in IL-18-induced Pulmonary Type-1, -2 and -17 Inflammation, Alveolar Destruction and Airway Fibrosis in the Murine Lung.. American Journal of Respiratory Cell and Molecular Biology. 2015;|
|Kang MJ, Yoon CM, Kim BH, Lee CM, Zhou Y, Sauler M, Homer R, Dhamija A, Boffa D, West AP, Shadel GS, Ting JP, Tedrow JR, Kaminski N, Kim WJ, Lee CG, Oh YM, Elias JA Suppression of NLRX1 in chronic obstructive pulmonary disease.. Journal of Clinical Investigation. 2015; 125 (6) : 2458-62.|
My role in basic and clinical research has largely derived from my position as Director of the Molecular Biology Core in the Section of Pulmonary Medicine. In that capacity, I have generated and characterized lung-specific overexpressing transgenic and null mutant mice to study in vivo roles and the effect of various cytokines in the pathogenesis of asthma, acute lung injury, pulmonary vascular disease, pulmonary fibrosis and emphysema.
KDDF-Bioneer-201312-11 (Lee/Chae) 2/11/2014- 10/10/2015
Korea Drug Development Fund (KDDF) $227,273
Selection of optimized lead compounds for preclinical studies for idiopathic pulmonary fibrosis using a novel RNAi-based nanoparticle technology SAMiRNA
Bioneer, a biotech company in Korea, developed Self Assembled Micelle-inhibitory RNA (SAMiRNA) technology as a novel and effective siRNA delivery method. In this project, the effectiveness of this SAMiRNA approach against pulmonary fibrosis will be determined through a variety of in vivo and in vitro evaluations and also using TGF-b transgenic mice developed by our laboratory as an animal model of pulmonary fibrosis. Thus, successful completion of this project will lead to the development of new drug for the effective intervention of pulmonary fibrosis.
Role: Principal Investigator
1 R01 HL115813-01A1 (Lee) 7/1/14 – 6/31/18
NIH / NHLBI $254,707
Chitinase 1 as a Biomarker and Therapeutic Target in Scleroderma Lung Disease
This grant proposes to define the roles and effects of chitinase1 in the pathogenesis of Scleroderma-associated interstitial lung disease. The studies in this project will evaluate the levels of chitinase1 in the blood or tissues of Scleroderma patients and controls to identify chitinase1 as a potential biomarker or a therapeutic target for this disease.
Role: Principal Investigator
1U01 HL 108638-01 (Elias) 8/15/11 – 6/30/15
NIH / NHLBI $396,455
YKL-40 in Idiopathic Pulmonary Fibrosis and Kidney Transplantation
This grant is designed to evaluate circulating YKL-40 as a biomarker for disease progression in IPF and urinary YKL-40 as a predictor of delayed graft function after renal transplantation. These studies will also evaluate the utility of YKL-40 as a therapeutic target in both disorders.
P01 HL114501-01A1 (Choi) 4/1/13 – 3/31/18
NIH / NHLBI $225,000
Distinct and Overlapping Pathways of Fibrosis and Emphysema in Cigarette Smokers
The focus is on the mechanisms that underlie the observation that cigarette smoke exposure and TGF-1 can contribute to the pathogenesis of COPD and IPF. Project 3 is based on evaluations of 10 different inbred murine backgrounds which define genetic modifiers that likely determine if TGF-1 causes fibrosis versus emphysema. These studies will define the expression of these modifiers in COPD and IPF and will define their roles in these biologic responses.
Role: Co-PI, Project 2
5 U01 HL108634 (Zhou/Elias) 9/1/13- 8/31/14 .
MAPGen Knowledge Base (MAPGenKB) and Coordination Center
In this ancillary project, we will measure the levels of YK-40 in patients with atherosclerosis, hypertension, metabolic syndromes and visceral fat accumulation. In addition, we will evaluate the roles of cell cycle regulation and the mitochondrial function in animal model of the diseases.
1 UH2 HL 123876-01 (Chupp/Elias) 7/1/14 – 6/30/19
Preclinical Development of a Novel Anti-YKL-40 Biologic to Treat Severe Asthma
We will complete the pre-clinical development of a humanized monoclonal antibody against the chitinase-like-protein, YKL-40, for the treatment of severe asthma. A companion diagnostic test will also be developed to measure YKL-40 in the serum that is drug-bound or free for monitoring the bioavailability, dosing, and biologic effect. The results will generate a novel therapeutic against a validated mediator of inflammation and remodeling in asthma and will lead to an Investigational New Drug (IND) application following the conclusion of the award.
NIH/ NHLBI 10/1/14 to 9/30/15
R56 HL 119511-01A1 (Bridge Award) (Kang)
NLRX1 and MAVS in cigarette smoke-induced inflammation and alveolar remodeling
The goal of this grant is to define the roles of novel mitochondrial molecules called NLRX1 and MAVS in the development of COPD. In addition, we will explore whether interventions that restore suppressed NLRX1 or modulate this pathway have therapeutic potential in a murine COPD model.
1981-1993 Full scholarship from Hanyang University for undergraduate and graduate courses, Hanyang
University, School of Medicine, Seoul Korea
1992-1993 Scholarship from Korean Public Health Institution, Seoul Korea
2005 Innovative Research Award, American Thoracic Society
1987 – 1992 Teaching Assistant, Hanyang University School of Medicine
1993 – 1995 Research Scientist, Division of Biotechnology, Korea National Institute of Health (KNIH)
1995 – 1996 Full-time Instructor, Hanyang University School of Medicine
1997 – 1998 Visiting fellow, LMM, NIAID, NIH
1998 – 1999 Post-doctoral fellow, Yale University School of Medicine
2000 – 2001 Associate Research Scientist, Yale University School of Medicine
2002 – 2007 Assistant Professor of Medicine, Yale University School of Medicine
2007 – 2009 Visiting Professor, Hanyang University School of Medicine
2002 - 2014 Director, Molecular Biology Core, Section of Pulmonary, Critical Care & Sleep Medicine, Yale University School of Medicine, New Haven, CT
2008 – 2014 Associate Professor of Medicine, Yale University School of Medicine
2014 – Present Professor, Dept of Molecular Microbiology and Immunology,
Division of Biology and Medical Sciences, Brown University