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Contact Information
Guo-Hua Fong, Ph.D.
Center for Vascular Biology
University of Connecticut Health Center
263 Farmington Avenue
Farmington, CT 06030-3501

Phone: 860-679-2373
Fax: 860-679-1201
Email: fong@nso2.uchc.edu

Fong Lab

 

Lab Members
Guo-Hua Fong
Principle Investigator
Email: fong@nso2.uchc.edu

Li-Juan Duan

Research Associate
Email: duan@neuron.uchc.edu
Vivienne Ho
Graduate Student
Email: vho@student.uchc.edu

Feng Qin

Graduate Student
Email: fqin@student.uchc.edu
Yifan Zhang
Graduate Student
Email: yizhang@student.uchc.edu
Research Interests

Many vascular diseases are results of inappropriate reactivation of the same mechanisms that are essential for the development of blood vessels during embryogenesis. Accordingly, our main interest is to understand how the development of the vascular system is controlled in mouse embryos.

In general, blood vessel growth is triggered by hypoxic conditions in tissues. Lack of oxygen results in the accumulation of hypoxia inducible factor-1α and -2α (HIF-1α and -2α), both of which can upregulate the expression of the vascular endothelial growth factor-A (VEGF-A). VEGF-A regulates vascular development by interactions with a number of receptors, two of which are transmembrane tyrosine kinases Flt-1 (VEGFR-1) and Flk-1/KDR (VEGFR-2). We are investigating how VEGF-A receptors regulate vascular development in mouse embryos, with an extended interest in how these receptors coordinate with each other during both embryonic development and tumor angiogenesis.

Besides activating the expression of VEGF-A, HIF-1α and -2α may also have other functions in supporting the growth of blood vessels. Therefore, we are also studying how HIF-2α might control the development and maturation of the vascular system in mouse embryos by a mechanism that may be complementary to the induction of VEGF-A expression.

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Lab Methods

Our main approach is to introduce genetic modifications into the mouse genome, analyze the phenotypic consequences in vascular development and deduce possible mechanisms underlying developmental defects. We maintain a within-the-lab ES cell facility and construct mouse embryos directly from modified ES cells by tetraploid as well as diploid aggregation. This approach often allows us to bypass the need of germline transmission.

Other methods employed in our research include immunohistochemistry and imaging techniques such as confocal microscopy. In addition, we employ recent molecular biology tools such as RNA interference and BAC cloning to speed up the process of modifying gene expression in ES cells or mouse embryos.

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