Huiyan Zeng, Ph.D.
Instructor of Medicine
Beth Israel Deaconess Medical Center
Harvard Medical School

330 Brookline Avenue, RN-270F
Boston, MA 02215
Office: 617-667-2329
Fax: 617-667-3591


Huiyan Zeng earned her Ph.D. in Division of Molecular Medicine, Department of Pharmacology, Boston University Medical Center, MA in 1998. She performed Postdoctoral training / NIH/NCI Postdoctoral fellowship (NRSA) at Beth Israel Deaconess Medical Center / Harvard Medical School with Dr. Debabrata Mukhopadhyay. In 2002, Dr. Zeng was appointed as an Instructor in Department of Pathology, Beth Israel Deaconess Medical Center / Harvard Medical School and obtained her NIH/NCI career development award. Later, she became an Assistant professor.

Research Interests: Molecular mechanism and signaling pathways in pathological angiogenesis


Basic Research - The research in my laboratory focuses on the molecular mechanism and signaling pathways that regulate pathological angiogenesis. My early work focused on the VEGF signaling in angiogenesis.  This work distinguished different signaling pathway of VEGF in endothelial cell proliferation and migration. More recent studies in my laboratory focused on function and molecular mechanism of downstream targeted genes of diseases involving angiogenesis, including tumor growth and metastasis, inflammation, and ischemia.  In particular, our emphasis has been on orphan nuclear receptor TR3 (mouse homolog Nur77) and Down Syndrome Candidate Region 1 isoform 1L (DSCR1-1L) that are critical factors for VEGF-induced endothelial cell proliferation, microvessel permeability and angiogenesis. Tumor growth were greatly inhibited in Nur77 knockout mice.
In order to better understand that mechanism that TR3/Nur77 and DSCr1-1L regulates pathological angiogenesis. We generated transgenic mice that Nur77 or DSCR1-1L is expressed inducibly and specifically in mouse endothelium. We have demonstrated that TR3/Nur77 regulates angiogenesis in the early stage to induce that formation of mother vessel and microvessel permeability by destabilization of endothelial junction. We have ongoing project to study the signaling pathways that regulates TR3 expression and molecular mechanism that TR3/Nur77 regulates angiogenesis.  We also have projects to study the function of TR3/Nur77 and DSCR1-1L in wound healing, inflammation and ischemia.   

Another project in my laboratory is to study the role of protein kinase D in VEGF-induced angiogenesis. We demonstrate that PKD interacts with PLCg and becomes tyrosine phosphorylated upon VEGF stimulation, leading to PLCg activation and angiogenic response of VEGF.

New and Noteworthy Publications:

Qin L, Zhao D, Xu J, Ren X, Terwilliger EF, Parangi S, Lawler J, Dvorak HF, Zeng H, The vascular permeabilizing factors histamine and serotonin induce angiogenesis through TR3/Nur77 and subsequently truncate it through thrombospondin-1. BLOOD 2013 Mar 14;121(11):2154-64

Zhao D, Qin L, Bourbon PM, James L, Dvorak HF, Zeng H Orphan nuclear transcription factor TR3/Nur77 regulates microvessel permeability by targeting endothelial nitric oxide synthase and destabilizing endothelial junctions. Proc Natl Acad Sci U S A. 2011 Jul 19; 108(29):12066-71. (PNAS direct submission)

Liu X, Zhao D, James L, Li J. Zeng H, Requirement of the nuclear localization of Transcription enhancer factor 3 (TEF3) for proliferation, migration, tube formation and angiogenesis induced by vascular endothelial growth factor (VEGF) FASEB J . 2011 25: 1188

$Zeng H, Qin LL, Zhao D, Tan X, Manseau EJ, Hoang MV, Senger DR, Brown LF, Nagy JA, Dvorak HD. Orphan Nuclear Receptor TR3/Nur77 regulates the early steps of VEGF-A-induced angiogenesis through its transcriptional activity. J Exp Med. 2006, 203: 719-729 ($Corresponding author)

Qin LL, Zhao D, Liu L, Nagy JA, Hoang MV, Brown LF, Dvorak HF, Zeng H. Down Syndrome Candidate Region 1 Isoform 1 (DSCR1-1L)-mediates angiogenesis through the Calcineurin-NFAT pathway. Mol Cancer Res. 2006, 4, 811-820