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Laboratory of Eunsil Hahm, PhD

Research interests in the laboratory of Eunsil Hahm, PhD are focused on understanding the chronic kidney disease (CKD) process, its etiology, pathology, and molecular mechanisms. Hahm has been trained in immunology and working in the fields of pharmacology and cell/molecular biology, with specific training and expertise in handling hematopoietic cells and experimental mice. Using several rodent models of CKD, and immunological approaches such as bone marrow transplantation (BMT), adoptive cell transfer, cell depletion, the Hahm laboratory was able to identify the functional connection between bone marrow and the kidney. And these novel findings implicate that bone marrow dysfunction might be one of the culprits for certain forms of CKD such as focal segmental glomerulosclerosis (FSGS) and diabetic nephropathy (DN). In addition, her laboratory is specially interested in developing a novel animal model of FSGS using the technology of humanized mice. This may help us to better understand the complexity of human kidney disease processes and could be beneficial in clinical applications onto the patient with FSGS in the future.

Hahm’s laboratory is housed within the Department of Internal Medicine.

Our work

Plasma soluble urokinase receptor (suPAR) has been suggested as a cause of FSGS (Wei C et al Nat Med 2011) and as a risk factor for future CKD in a large observational study (Hayek et al. NEJM 2015). Hahm and her collaborators found that bone marrow myeloid progenitor cells are responsible for production of pathological suPAR, resulting in kidney damage and proteinuria (manuscript under review). This work included significant collaborations with Jochen Reiser, MD, PhD (suPAR) at RUSH and David Scadden, MD (stem cell) at Massachusetts General Hospital (MGH) and Harvard Stem Cell Insititute.

Other work

Other research project collaborating with Vineet Gupta, PhD at RUSH aims to develop novel therapeutic agents that target and stabilize podocytes as a strategy for the treatment of proteinuric kidney disease. For this project, the Hahm laboratory uses the humanized rodent model of kidney disease to validate identified hit compounds.


Hahm’s research has been funded by the National Institutes of Health through grants collaboratively submitted with Dr. Reiser (R01, a humanized mouse model of FSGS) and with Vineet Gupta, PhD (R01, Novel Anti-Proteinuric Strategies Targeting Podocytes).   


Abstract Achievement Award, 53rd Annual Meeting of American Society of Hematology (2011)


A complete list of her journal articles can be found on PubMed.

Selected Publications

1. Li J, Kim K, Hahm E, Molokie R, Hay N, Gordeuk V, Du X, Cho J. Neutrophil Akt2 regulates heterotypic neutrophil-platelet interactions during vascular inflammation. J Clin Invest. 2014 Apr;124(4):1483-96.
2. Kim K, Hahm E, Li J, Holbrook LM, Sasikumar P, Stanley RG, Ushio-Fukai M, Gibbins JM, Cho J. Platelet protein disulfide isomerase is required for thrombus formation but not for hemostasis in mice. Blood. 2013 Aug 8;122(6):1052-61.
3. Hahm E, Li J, Kim K, Hur S, Rogelj S, Cho J. Extracellular protein disulfide isomerase regulates ligand binding activity of M2 integrin and neutrophil recruitment during vascular inflammation. Blood. 2013 May 9;121(19):3789-800. (Plenary Paper)
4. Lu SJ, Li F, Yin H, Feng Q, Kimbrel EA, Hahm E, Thon JN, Wang W, Italiano JE, Cho J, Lanza R. Platelets generated from human embryonic stem cells are functional in vitro and in the microcirculation of living mice. Cell Res. 2011 Mar;21(3):530-45.
5. Lee SK, Kang JS, Jung DJ, Hur DY, Kim JE, Hahm E, Bae S, Kim HW, Kim D, Cho BJ, Cho D, Shin DH, Hwang YI, Lee WJ. Vitamin C suppresses proliferation of the human melanoma cell SK-MEL-2 through the inhibition of cyclooxygenase-2 (COX-2) expression and the modulation of insulin-like growth factor II (IGF-II) production. J Cell Physiol. 2008 Jul;216(1):180-8.
6. Hahm E, Lee YS, Jun HS. Suppressive effects of glucagon-like peptide-1 on interferon-gamma-induced nitric oxide production in insulin-producing cells is mediated by inhibition of tumor necrosis factor-alpha production. J Endocrinol Invest. 2008 Apr;31(4):334-40.
7. Hahm E, Jin DH, Kang JS, Kim YI, Hong SW, Lee SK, Kim HN, Jung DJ, Kim JE, Shin DH, Hwang Y, Kim YS, Hur DY, Yang Y, Cho D, Lee M, Lee WJ. The molecular mechanisms of vitamin C on cell cycle regulation in B16F10 murine melanoma. J Cell Biochem. 2007 Apr 23;102(4):1002-10.
8. Lee YS, Shin S, Shigihara T, Hahm E, Liu M-J, Han J, Yoon JW, Jun HS. Glucagon-like peptide-1 gene therapy in obese diabetic mice results in long-term cure of diabetes by improving insulin sensitivity and reducing hepatic gluconeogenesis. Diabetes 2007 Jun;56(6):1671-9.


Eunsil Hahm, PhD
Assistant Professor

Rush University
Department of Internal Medicine
Cohn Research Building
1735 W. Harrison St., Room 726
Chicago, IL 60612

Phone: (312) 942-0357