Rong Wang, PhD

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Rong Wang, PhD

Professor, Department of Surgery, UCSF; Director, Laboratory for Accelerated Vascular Research
Mildred V. Strouss Endowed Chair in Vascular Surgery, UCSF

rong.wang@ucsf.edu

Phone: (415) 476-6855
Box 0222, 513 Parnassus Ave, 1618
San Francisco, CA 94143

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Research Summary

Angiogenesis, or new blood vessel formation, plays a principal role in health and cancer. Research in my lab aims to advance the fundamental understanding of the cellular, molecular, and hemodynamic mechanisms underlying arterial venous programming in normal and tumor angiogenesis. We are well equipped to perform state-of-the-art research at the organismic, cellular, and molecular levels. Sophisticated mouse genetics allow us to delete or express genes in endothelial cells that line the vessel lumen in a lineage-specific and temporally controllable fashion. These mouse tools are enhanced with cutting-edge imaging capabilities, including 5D two-photon microscopy (3D + blood flow over time). These innovations provide us exceptional access to in vivo cell biology and gene function in both physiological and pathological angiogenesis in living animals. This basic approach is complemented by preclinical studies with our elegant mouse models of disease, offering outstanding opportunities for early translational research. With these approaches, we are investigating the molecular programming in the development of arteries in hepatocellular carcinoma (HCC), which is characterized by highly arterialized tumor masses.

We hypothesize that genes important in normal arterial programming are likely to play a role in HCC artery formation, and we intend to ultimately study the Notch pathway as a molecular regulator of HCC arterial formation. Our goal is to inhibit HCC arterial growth, block tumor blood supply, and starve cancer cells. Our investigation of the molecular regulators that govern arterial-venous programming may ultimately help identify novel drug targets and inform rational design of new therapeutics to treat major human diseases, including HCC. I have many years of experience studying HCC in mouse models, beginning with my postdoctoral research. I pioneered the liver-specific tetracycline-regulatable Met transgenic mouse model of HCC and contributed to the development of the hydrodynamic injection HCC mouse model, both currently in wide use. The combination of my expertise in HCC and my broad experience in arterial-venous programming prepare us well to investigate the effects of targeting the arterial supply of HCC.

Education

Sichuan University, Chendu, China, B.Sc., 1980-84, Biology
Graduate School of Chinese Science and Technology University, Institute of Genetics, Academia Sinica, Beijing, China, M.Sc. candidate, 1984-88, Genetics
University of North Carolina at Chapel Hill, Ph.D., 1988-93, Biology (Angiogenesis)
University of California, San Francisco, Postdoctoral Fellow, 1994-2001, Cancer Biology


Professional Experience

  • 1988-1993
    Graduate Research Assistant, Dr. Victoria L. Bautch, Department of Biology, University of North Carolina at Chapel Hill
  • 1994-2001
    Postdoctoral Fellow, J. Michael Bishop, G.W. Hooper Laboratory, UCSF
  • 2001-2007
    Assistant Professor, Surgery and Anatomy, UCSF
  • 2001-present
    Director, Laboratory for Accelerated Vascular Research, UCSF
  • 2006-present
    Mildred V. Strouss Endowed Chair in Vascular Surgery
  • 2007-2008
    Associate Professor, Anatomy, UCSF
  • 2007-2015
    Associate Professor, Surgery, UCSF
  • 2015-present
    Professor, Surgery, UCSF

Honors & Awards

  • 1994-97
    Leukemia Society of America, Postdoctoral Fellowship
  • 1997-99
    American Heart Association, Postdoctoral Fellowship
  • 2003-2005
    Pfizer Atorvastatin Research Award

Selected Publications

  1. Mouse Models of Cerebral Arteriovenous Malformation. Stroke. 2016 Jan; 47(1):293-300.
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  2. Constitutively active Notch4 receptor elicits brain arteriovenous malformations through enlargement of capillary-like vessels. Proc Natl Acad Sci U S A. 2014 Dec 16; 111(50):18007-12.
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  3. Endothelial ephrin-B2 is essential for arterial vasodilation in mice. Microcirculation. 2014 Oct; 21(7):578-86.
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  4. Deletion of Rbpj from postnatal endothelium leads to abnormal arteriovenous shunting in mice. Development. 2014 Oct; 141(19):3782-92.
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  5. Molecular identification of venous progenitors in the dorsal aorta reveals an aortic origin for the cardinal vein in mammals. Development. 2014 Mar; 141(5):1120-8.
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  6. Notch4 is required for tumor onset and perfusion. Vasc Cell. 2013; 5(1):7.
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  7. Line-scanning particle image velocimetry: an optical approach for quantifying a wide range of blood flow speeds in live animals. PLoS One. 2012; 7(6):e38590.
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  8. Notch4 normalization reduces blood vessel size in arteriovenous malformations. Sci Transl Med. 2012 Jan 18; 4(117):117ra8.
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  9. Constitutively active endothelial Notch4 causes lung arteriovenous shunts in mice. Am J Physiol Lung Cell Mol Physiol. 2010 Feb; 298(2):L169-77.
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  10. Arterial-venous segregation by selective cell sprouting: an alternative mode of blood vessel formation. Science. 2009 Oct 9; 326(5950):294-8.
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  11. Endothelial Notch signaling is upregulated in human brain arteriovenous malformations and a mouse model of the disease. Lab Invest. 2009 Sep; 89(9):971-82.
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  12. Cellular and molecular mechanism regulating blood flow recovery in acute versus gradual femoral artery occlusion are distinct in the mouse. J Vasc Surg. 2008 Dec; 48(6):1546-58.
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  13. Artery and vein size is balanced by Notch and ephrin B2/EphB4 during angiogenesis. Development. 2008 Nov; 135(22):3755-64.
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  14. Endothelial Notch4 signaling induces hallmarks of brain arteriovenous malformations in mice. Proc Natl Acad Sci U S A. 2008 Aug 5; 105(31):10901-6.
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  15. Placental rescue reveals a sole requirement for c-Myc in embryonic erythroblast survival and hematopoietic stem cell function. Development. 2008 Aug; 135(14):2455-65.
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  16. c-myc in the hematopoietic lineage is crucial for its angiogenic function in the mouse embryo. Development. 2008 Aug; 135(14):2467-77.
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  17. Cell-autonomous requirement for beta1 integrin in endothelial cell adhesion, migration and survival during angiogenesis in mice. Development. 2008 Jun; 135(12):2193-202.
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  18. Distinct pathways of genomic progression to benign and malignant tumors of the liver. Proc Natl Acad Sci U S A. 2007 Sep 11; 104(37):14771-6.
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  19. Endothelial FAK is essential for vascular network stability, cell survival, and lamellipodial formation. J Cell Biol. 2006 Jan 2; 172(1):151-62.
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  20. Optimization of adenovirus-mediated endothelial nitric oxide synthase delivery in rat hindlimb ischemia. Gene Ther. 2005 Nov; 12(22):1640-50.
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