Kyu-Ho Lee

Kyu-Ho Lee, M.D., Ph.D.
Assistant Professor

Pediatrics (Cardiology), MUSC Children's Hospital
Obstetrics/Gynecology, MUSC
Adjunct Faculty, Regenerative Medicine and Cell Biology, MUSC
Adjunct Faculty, Bioengineering Department, Clemson University

Office: Room 615, Children's Research Institute, (843) 792-0307
Email: leekh@musc.edu

Lab Members and Pictures
Visitors to the Laboratory


SB, Massachusetts Institute of Technology 1984
MD, PhD John Hopkins University 1992
Residency in Pediatrics, Boston Children’s Hospital
Fellowship and Postdoctoral Training, Boston Children’s Hospital / Harvard Medical School

Research Interests:

The Lee Lab currently has an available position for a graduate student or postdoctoral fellow. Interested candidates should forward CV and a short letter of research interests to leekh@musc.edu.

Children’s Heart Program of South Carolina
MUSC Children’s Hospital
Tinman Article in MUSC Progress Notes

The Lee Laboratory, in the Departments of Pediatrics at MUSC Children’s Hospital, investigates two major disease areas affecting child and maternal health: Congenital heart disease (CHD), which affects approximately 1% of live births; and preeclampsia or hypertension in pregnancy, which occurs in 3-5% of pregnancies.

fig 1
These efforts revolve around the genetic pathways leading to and emanating from the early cardiac transcription factor, Nkx2-5. Missense sequence variants of Nkx2-5 are associated with about 4% of human CHD, and altered Nkx2-5 expression levels in experimental mice has a profound effect on development of the Second Heart Field (SHF), a distinct set of heart precursors which gives rise to outflow tract (OFT), right ventricle and atrial septal regions of the developing heart.

Congenital heart disease research utilizes several transgenic mouse tools developed as part of our past research on the conserved regulation of Nkx2-5 in the SHF in vertebrates, which allow for identification of SHF progenitor lineages, and cell-type specific knockout of genes important for OFT development.

fig 2
Preeclampsia research currently focuses on recent novel findings of abnormally high levels of Nkx2-5 expression in placental tissue from women suffering from a severe form of preeclampsia, in association with altered expression of anti-angiogenic factors that are emerging clinical biomarkers for preeclampsia.

These efforts focus upon investigation of functional linkages between Nkx2-5-driven anti-angiogenic factor and modifier gene expression, expanded patient profiling to determine the overall prevalence of an “Nkx2-5 signature” in the preeclampsia population, and the testing of animal models which use transgenic tools to alter expression of Nkx2-5 and related pathway genes in placental trophoblast lineages.


Complete list of publications on MyNCBI

  1. Lauriol J, Cabrera JR, Roy A, Keith K, Hough SM, Damilano F, Wang B, Segarra GC, Flessa ME, Miller LE, Das S, Bronson R, Lee KH, Kontaridis MI. Developmental SHP2 dysfunction underlies cardiac hypertrophy in Noonan syndrome with multiple lentigines. J Clin Invest. 2016 Jun 27. pii: 80396. doi: 10.1172/JCI80396. [Epub ahead of print] PMID:
  2. Rivers ER, Horton AJ, Hawk AF, Favre EG, Senf KM, Nietert PJ, Chang EY, Foley AC, Robinson CJ, Lee K.H. Placental Nkx2-5 and target gene expression in early-onset and severe preeclampsia. Hypertens Pregnancy. 2014 Jul 2:1-15. PMID: 24987805
  3. Clark, C. D., Zhang, B., Lee, B., Evans, S. I., Lassar, A. B., and LeeK. H. (2012) Evolutionary Conservation of Nkx2.5 Autoregulation in the Second Heart Field. Dev. Biol. 374 (1):198-209. PMCID: PMC3549048
  4. Brody, M. J., Mysliwiec, M. R., Kim, T. G., Carlson, C. D., Cho, E. Lee, K. H. and Lee, Y. S. (2013) Lrrc10 is a novel cardiac-specific target gene of Nkx2-5 and GATA4. J. Molec. Cell Cardiol. S0022-2828 (13): 198-203. PMID: 23751912.
  5. Barth, J.L., Clark, C.D., Fresco, V.M., Knoll, E.P., Lee, B., Argraves, W.S., and Lee, K.H. (2010). Jarid2 is among a set of genes differentially regulated by Nkx2.5 during outflow tract morphogenesis. Dev Dyn 239, 2024-2033.
  6. Ikeda, S., He, A., Kong, S.W., Lu, J., Bejar, R., Bodyank, N., Lee, K.H., Ma, Q., Kang, P., Golub, T., and Pu, W.T. (2009) microRNA-1 attenuates cardiomyocyte hypertrophy by negatively regulating calmodulin and Mef2a. Mol. Cell. Biol. 29(8):2193-204.
  7. Rivera-Feliciano, J., Lee, K.H., Kong, S.W., Ma, Q., Springer, Z., Izumo, S., Tabin, C.J. and Pu, W.T. (2006) Development of heart valves requires Gata4 expression in endocardium derived cells. Development 133(18): 3607-18.
  8. Lee, K. H., Evans, S., Ruan, T. Y., and Lassar, A. B. (2004). Smad-mediated modulation of YY1 activity regulates the BMP response and cardiac-specific expression of a GATA-4,-5,-6 dependent chick Nkx-2.5 enhancer. Development 131: 4709-4723.
Last updated on 28-Dec-2017

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