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  • Associate Professor, The Center for Biomedical Science, Feinstein Institutes for Medical Research

About the investigator

Dr. Yang obtained an MD in China in 1983 and a PhD at the University of Wisconsin-Madison in 1993. Dr. Yang obtained further 5-year post-doctoral training in the Department of Biochemistry in San Antonio Texas, followed by training at the NIH, National Institute of Aging, Baltimore, MD. In 1998, Dr. Yang joined the research group of Dr. Kevin J. Tracey at The Feinstein Institutes for Medical Research and began her studies on cytokines and sepsis.

Dr. Yang has published over 59 peer-reviewed papers, many of which are in high impact journals; and she is a co-inventor of two patents. Dr. Yang has been an invited speaker at many national and international meetings, including The International Endotoxin Society Meeting, American Thoracic Society 99th International Conference, The HMGB1 Congress, World Congress on Trauma, Shock, Inflammation and Sepsis, The 11th Congress of the European Shock Society, Society of Critical Care Medicine Annual Congress. Dr. Yang has also served as a journal reviewer for Critical Care MedicineExpert Opinion on Therapeutic TargetAmerican Journal of the Medical SciencesArthritis Research and Therapy, Food and chemical toxicology.

Research focus

Dr. Yang‘s research interest is on inflammation and sepsis. She has especially focused her work on a novel and exciting cytokine-like molecule called HMGB1. HMGB1 is integral in amplifying inflammation. Currently, Dr. Yang and her team are working on the molecular basis of HMGB1 and its receptor interaction, in order to study how does HMGB1 function as a cytokine. In collaboration with Drs. Kevin J. Tracey and Yousef Al-Abed, Dr. Yang showed that in carrying out its pro-inflammatory functions, TLR4/MD2 receptors have subtle but distinctly different structural requirements for HMGB1, adding to the specificity of events within this broad canvas of inflammation.

In addition, Dr. Yang and her team are using DNA-conjugated beads to sequester HMGB1 in murine colitis in mice, as HMGB1 acts as a cytokine mediator of inflammation in the pathogenesis of inflammatory bowel disease (IBD). Since HMGB1 binds to DNA with high affinity, Dr. Yang has developed oligonucleotides immobilized onto sepharose beads and used them as a novel agent to sequester HMGB1 in treatment of IBDs. Dr. Yang and her team observed that oral administration of DNA-containing beads reduced the weight loss of IL-10 knockout mice with spontaneous colitis, ameliorated colon injury, reduced levels of serum HMGB1 compared with mice treated with empty beads (no DNA). This data suggest a therapeutic potential for DNA beads to sequester HMGB1 in inflammatory bowel diseases.

Dr. Yang has been collaborating with Dr. Kevin J. Tracey and members of Tracey Lab, Drs. Haichao Wang, Yousef Al-Abed, Lionel BlancBetty DiamondJesse RothPing Wang and many scientists outside the Feinstein Institutes.

Lab members

Joan Zeng, PhD
Research Scientist
Email[email protected]
Phone: (516) 562-2109


University of Wisconsin-Madison, Department of Nutritional Sciences, Madison, WI
Degree: PhD

Hubei Medical College, P.R. China
Degree: MD
Field of study: Medicine

Honors & awards

  • 2011 Research grant from National Institute of General Medical Sciences, NIH
  • 2007 Fellowship Award, KeySpan Corporation, Hicksville, NY
  • 1995 Intramural Research Training Award for post-doctoral fellowship, National Institute of Health, Baltimore, MD
  • 1993 Post-doctoral fellowship award from San Antonio Cancer Institute, San Antonio, TX


  1. Yang, H., D. J. Antoine, U. Andersson and K. J. Tracey (2013). “The many faces of HMGB1: molecular structure-functional activity in inflammation, apoptosis, and chemotaxis.” Journal of leukocyte biology 93(6): 865-873. PMCID: PMC4051189
  2. Ju, Z., S. S. Chavan, D. J. Antoine, M. Dancho, T. Tsaava, J. Li, B. Lu, Y. A. Levine, A. Stiegler, Y. Tamari, Y. Al-Abed, J. Roth, K. J. Tracey and H. Yang (2014). “Sequestering HMGB1 via DNA-conjugated beads ameliorates murine colitis.” PLoS One 9(8): e103992. PMCID: PMC4134190
  3. Lu, B., D. J. Antoine, K. Kwan, P. Lundback, H. Wahamaa, H. Schierbeck, M. Robinson, M. A. Van Zoelen, Yang, J. Li, H. Erlandsson-Harris, S. S. Chavan, H. Wang, U. Andersson and K. J. Tracey (2014). “JAK/STAT1 signaling promotes HMGB1 hyperacetylation and nuclear translocation.” Proc Natl Acad Sci USA 111(8): 3068-3073. PMCID: PMC3939889
  4. Lu, B, K. Kwan, Y. A. Levine, P. S. Olofsson, Yang, J. Li, S. Joshi, H. Wang, U. Andersson, S. S. Chavan and K. J. Tracey (2014). “α7 nicotinic acetylcholine receptor signaling inhibits inflammasome activation by preventing mitochondrial DNA release.” Mol Med 20: 350-358. PMCID: PMC4153835
  5. Li, W., S. Zhu, J. Li, J. D’Amore, J. D’Angelo, Yang, P. Wang, K. J. Tracey and H. Wang (2015). “Serum Amyloid A Stimulates PKR Expression and HMGB1 Release Possibly through TLR4/RAGE Receptors.” Mol Med 21: 515-525. PMCID: PMC4607615
  1. Liesz, A., A. Dalpke, E. Mracsko, D. J. Antoine, S. Roth, W. Zhou, Yang, S. Y. Na, M. Akhisaroglu, T. Fleming, T. Eigenbrod, P. P. Nawroth, K. J. Tracey and R. Veltkamp (2015). “DAMP signaling is a key pathway inducing immune modulation after brain injury.” J Neurosci 35(2): 583-598. PMCID: PMC4293412
  2. Pribis, J. P., Y. Al-Abed, Yang, D. Gero, H. Xu, M. F. Montenegro, E. M. Bauer, S. Kim, S. S. Chavan, C. Cai, T. Li, P. Szoleczky, C. Szabo, K. J. Tracey and T. R. Billiar (2015). “The HIV protease inhibitor saquinavir inhibits HMGB1 driven inflammation by targeting the interaction of cathepsin V with TLR4/MyD88.” Mol Med 21(1): 749–757. PMCID: PMC4749497
  3. Yang, H., H. Wang, S. S. Chavan and U. Andersson (2015). “High Mobility Group Box Protein 1 (HMGB1): The Prototypical Endogenous Danger Molecule.” Mol Med 21(Suppl1): S6-S12. PMCID: PMC4661054
  4. Yang, H., H. Wang, Z. Ju, A. A. Ragab, P. Lundback, W. Long, S. I. Valdes-Ferrer, M. He, J. P. Pribis, J. Li, B. Lu, D. Gero, C. Szabo, D. J. Antoine, H. E. Harris, D. T. Golenbock, J. Meng, J. Roth, S. S. Chavan, U. Andersson, T. R. Billiar, K. J. Tracey and Y. Al-Abed (2015). “MD-2 is required for disulfide HMGB1-dependent TLR4 signaling.” J Exp Med 212(1): 5-14. PMCID: PMC4291531
  5. Yang, H., Wang H, Levine YA, Gunasekaran MK, Wang Y, Addorisio M, Zhu S, Li W, Li J, de Kleijn DP, Olofsson PS, Warren HS, He M, Al-Abed Y, Roth J, Antoine DJ, Chavan SS, Andersson U, Tracey KJ (2016). “Identification of CD163 as an antiinflammatory receptor for HMGB1-haptoglobin complexes.” JCI Insight 1(7). PMCID: PMC4902170
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