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Huiyan Zeng, PhD

Assistant Professor, Department of Medicine, Harvard Medical School

Assistant Professor, Medicine, Beth Israel Deaconess Medical Center

Contact Info

Huiyan Zeng
Beth Israel Deaconess Medical Center
99 Brookline Ave.

Boston, MA, 02215
Phone: 617-667-2329
Fax: 617-667-3591
hzeng@bidmc.harvard.edu

Assistant

Not Available.

DF/HCC Program Affiliation

Angiogenesis, Invasion and Metastasis

Research Abstract

The research in my laboratory focuses on the molecular mechanism and signaling pathways that regulate tumor angiogenesis. In gene profile studies of cultured endothelial cells exposed to VEGF-A165, we found that TR3 (mouse homologue, Nur77) was highly upregulated not only in VEGF-A165-stimulated endothelial cells, but also in microvessels in several examples of pathological angiogenesis in vivo, including adenovirus VEGF-A164-induced angiogenesis, skin wound healing and tumors. growth of B16 melanoma was completely inhibited in Nur77 knock out (nur77-/-) mice. Overexpression of TR3/Nur77 was sufficient by itself to induce angiogenesis and also that TR3/Nur77 had an essential role in VEGF-A165-induced angiogenesis.

Down syndrome candidate region 1 (DSCR1) is another gene that is identified to be upregulated by VEGF. DSCR1 can be expressed as four isoforms, one of which, isoform 4 (DSCR1-4), has recently been found to provide a negative feedback loop that inhibits VEGF-A165-induced endothelial cell proliferation in vitro and angiogenesis in vivo. We found that another DSCR1 isoform, DSCR1-1L, was also upregulated by VEGF-A165 in cultured endothelial cells and is strongly expressed in several types of pathological angiogenesis in vivo. Moreover, DSCR1-1L and DSCR1-4 were expressed in tumor microvascular structure, not in tumor cells, nor in normal vessel, either. DSCR1-1L, unlike DSCR1-4, potently activates angiogenesis and could be an attractive target for anti-angiogenesis therapy.

Another project 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-A165.

Publications

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