Pioneering Rehabilitation

Eunhee Kim, Ph.D.

Instructor, Preclinical Stroke Modeling

Brain and Mind Research Institute
Weill Cornell Medicine 


(914) 597-2157

Research Focus

A stroke is the loss of brain function due to a disturbance in the blood supply to the brain. This disturbance is caused by either ischemia (lack of blood flow) or hemorrhage (bleeding of blood vessels of the brain). Stroke is the major leading cause of disability and death worldwide, however, the treatment options are currently very limited.

My research interest is the neuroimmune system in ischemic stroke. I am particularly interested in the role of CD36, a scavenger receptor that has multiple roles—in lipid metabolism, innate immunity, and inflammation—in acute ischemic injury under hyperlipidemic condition.

Hyperlipidemia is a co-morbidity that increases the risk of stroke and worsens stroke outcome. In the hyperlipidemic condition, the CD36-mediated inflammatory response contributes to ischemic injury. Both periphery and brain CD36 have been shown to induce worsened ischemic outcomes in the hyperlipidemic condition. Based on these studies, I currently focus on the role of CD36 in peripheral pro- and anti-inflammatory monocyte/macrophage trafficking in the stroked brain and its effect on acute ischemic injury in the hyperlipidemic condition. 


Bachelor of Science, Feb. 2000
Applied Biology, Dongguk University, Seoul, Korea

Master of Science, Feb. 2003
Microbiology, Dongguk University, Seoul, Korea

Doctor of Philosophy, Feb. 2006
Neuroendocrinology/Pharmacology, School of Medicine, Kyunghee University, Seoul, Korea

Post-doctoral fellow, Mar. 2006—Aug. 2013
Winifred Masterson Burke Medical Research Institute, White Plains, New York, USA


Kim E, Tolhurst AT, Szeto HH, Cho S (2014) Targeting CD36-Mediated Inflammation Reduces Acute Brain Injury in Transient, but not Permanent, Ischemic Stroke. CNS Neurosci Ther. doi: 10.1111/cns.12326. [Epub ahead of print.]

Kim E, Yang J, Beltran CD, Cho S (2014) Role of Spleen-derived monocytes/macrophages in acute ischemic brain injury. J Cereb Blood Flow Metab, May 28. doi: 10.1038/jcbfm.2014.101. 

Kim E, Tolhurst AT, Cho S (2014) Deregulation of inflammatory response in the diabetic condition is associated with increased ischemic brain injury. J Neuroinflammation, May 1;11(1):83. doi: 10.1186/1742-2094-11-83. PMCID:PMC4017808.

Bao Y, Qin L, Kim E, Bhosle S, Guo H, Febbraio M, Haskew-Layton RE, Ratan R, Cho S. (2012) CD36 is involved in astrocyte activation and astroglial scar formation. J Cereb Blood Flow Metab. Aug;32(8):1567-77. doi: 10.1038/jcbfm.2012.52. Epub 2012 Apr 18. PMCID:PMC3421096.

Kim E, Febbraio E, Bao Y, Tolhurst AT, Epstein JM, Cho S. (2012) CD36 in the periphery and brain synergizes in stroke injury in hyperlipidemia. Ann Neurol, Jun; 71(6):753-64. PMCID:PMC3383818.

Basso M, Berlin J, Xia L, Sleiman S, Ko B, Haskew-Layton RE, Kim E, Antonyak M, Cerione R, Iismaa S, Willis D, Cho S, Ratan R. (2012) Transglutaminase inhibition protects against oxidative stress-induced neuronal death downstream of pathological ERK activation. J Neurosci. May 9;32(19):6561-9. PMCID:PMC3444816.

Qin L, Kim E, Ratan R, Lee FS, Cho S (2011) Genetic variant of BDNF (Val66Met) polymorphism attenuates stroke-induced angiogenic responses by enhancing anti-angiogenic mediator CD36 expression. J Neurosci. Jan 12;31(2):775-83. PMCID:PMC3308129.

Bao Y, Kim E, Bhosle S, Mehta H, Cho S (2010) A role for spleen monocytes in post-ischemic brain inflammation and injury. J Neuroinflammation Dec 15;7:92. PMCID:PMC3016273.

Cho S, Kim E CD36: A multi-modal target for acute stroke therapy (2009) J Neurochem. May;109 Suppl 1:126-32. PMCID:PMC2702148.

Kim E, Seo S, Chung H, Park S (2008) Role of Glucocorticoids in Fasting-induced Changes in Hypothalamic and Pituitary Components of the Growth Hormone (GH)-axis. Korean J Physiol Pharmacol. Oct;12(5):217-23. PMCID:PMC2788639.

Kim E, Tolhurst AT, Qin LY, Chen XY, Febbraio M, Cho S (2008) CD36/fatty acid translocase an inflammatory mediator, is involved in hyperlipidemia-induced exacerbation in ischemic brain injury. J Neurosci. Apr 30;28(18):4661-70. PMCID:PMC2830708.

Jung HJ, Kim EH, Mun JY, Park S, Smith ML, Han SS, Seo YR (2007) Base excision DNA repair defect in Gadd45a-deficient cells. Oncogene Nov 29;26(54):7517-25. PMID:17599061.

Cho S., Szeto H.H., Kim E., Kim H., Tolhurst A.T., Pinto J.T. (2007) A novel cell permeableantioxidant  peptide, SS31, attenuates ischemic brain injury by down-regulating CD36. JBC 282(7):4634-4642. PMID:17178711.

Chung H, Kim E, Lee DH, Seo S, Ju S, Lee D, Kim H, Park S. (2007) Ghrelin Inhibits Apoptosis in Hypothalamic Neuronal Cells during Oxygen-Glucose Deprivation. Endocrinology, Jan;148(1):148-59. PMID:17053024.

Kim E, Sohn S, Lee M, Jung J, Kineman RD, Park S. (2006) Differential responses of the GH-axis in two rat models of streptozotocin-induced insulinopenic diabetes. J Endocrinol., Feb; 188(2):263-70. PMID:16461552.

Kim E, Sohn S, Lee M, Park C, Jung J, Park S. (2005) Effect of gsp oncogene on somatostatin receptor subtype 1 and 2 mRNA levels in GHRH-responsive GH3 cells. Pituitary, 8(2):155-62. PMID:16379030.

Park C, Kim E, Sohn S, Yang I, Koh G, Oh S, Woo J, Kim S, Kim J, Kim Y, Oh K, Park S, Park S. (2005) Acute hyperglycemia and activation of the beta-adrenergic system do not exhibit synergistic inhibitory actions on thyrotropin-releasing hormone (TRH)-induced thyroid stimulating hormone (TSH) secretion. Endocr J., Feb;52(1):69-74. PMID:15758560.

Park C, Yang I, Woo J, Kim S, Kim J, Kim Y, Sohn S, Kim E, Lee M, Park H, Jung J, Park S. (2004) Pituitary adenomas: the relationship with endogenous srif activity and response to octreotide. Endocr J., Apr;51(2):227-36. PMID:15118275.

Current Projects

Role of CD36 in ischemic stroke with hyperlipidemia

Although stroke incidence and severity are both increased in patients with hyperlipidemia, the underlying mechanism(s) of the poor outcome is not clear. It is well known that hyperlipidemia is a chronic pro-inflammatory state. The goal of this project is to define how enhanced peripheral inflammation influences acute ischemic injury and what the role of CD36 is in the periphery-CNS immune mechanism after stroke in hyperlipidemic condition.

The persistent presence of monocytes/macrophages (MMs) in the infarct zone suggests that the MMs play a role in ischemia-induced brain inflammation and injury. Previously we have shown that CD36 regulates monocyte chemoattractant protein-1 (MCP-1) and CCR2, which are involved in MM mobilization. Two distinctive MM subsets have been reported: pro-inflammatory, expressing CCR2; and anti-inflammatory, not expressing CCR2. Hyperlipidemia expands the CCR2-expressing pro-inflammatory MM subsets in the periphery including the spleen.

In this project, I specifically investigate i) the role of spleen MMs in stroke-induced brain injury in hyperlipidemic conditions and ii) if CD36 regulates the CCR2 expressing MM mobilization to ischemic brain. Understanding the neuroimmune mechanism in stroke with hyperlipidemia may help narrow the gap between clinic and laboratory and provide a novel therapeutic strategy for stroke patients.  


Ongoing Research Support

National Institutes of Health/National Heart, Lung, and Blood Institute   
2R01 HL02511 (PI: Sunghee Cho, Ph.D.)
Role: Post-doctoral fellow  
Dates of project: 8/3/2011 — 6/30/2015         

Past Research Support

National Institutes of Health/National Heart, Lung, and Blood Institute     
R01HL082511 (PI: Sunghee Cho, Ph.D.)
Role: Post-doctoral fellow
Dates of project: 1/1/2006 — 7/31/2011