Matthew L. Springer, 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
Matthew L. Springer, PhD

Professor, Department of Medicine, UCSF

matt.springer@ucsf.edu

Phone: (415) 502-8404
Box 0124, UCSF
San Francisco, CA 94143-0124

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Cancer Center Membership

Program Member ยป Tobacco Control

Research Summary

Dr. Matthew L. Springer received his BA from the University of California, Berkeley in 1985 and his PhD from Stanford University in 1992. He did postdoctoral research at Stanford and continued his research there as a senior scientist until joining the UCSF faculty in 2003, where he is currently one of two non-clinicians on the faculty of the Division of Cardiology. The close juxtaposition of his basic research background with the clinical cardiologists in the Division has resulted in an active translational research program.

Dr. Springer's research interests include cell therapy and gene therapy approaches to studying cardiovascular disease, with the goals of exploring potential treatments and understanding underlying mechanisms involved in angiogenesis, vascular function, and treatments for myocardial infarction. The laboratory is studying the effects of VEGF and pleiotrophin gene therapy on the heart and limb vasculature in mice. Further interests center in the therapeutic effects of ultrasound-guided bone marrow cell implantation into the heart after myocardial infarction, with a special emphasis on the therapeutic implications of the age and cardiac disease state of the cell donor. Similarly, the lab is studying the effects of age and disease on circulating angiogenic cells (sometimes called endothelial progenitor cells), with a focus on the roles of endothelial nitric oxide synthase and nitric oxide in the function of these cells. Lastly, they have developed a rat model of endothelium-dependent flow-mediated vasodilation, and are using it to examine mechanisms underlying vascular reactivity and how they are affected by tobacco and marijuana secondhand smoke exposure.

Website: Springer Laboratory

Education

University of California, Berkeley, CA, B.A., 1981-1985, Molecular Biology
Stanford University, Stanford, CA, Ph.D., 1985-1991, Biological Sciences
Stanford University, Stanford, CA, (postdoctoral), 1991-1993, Cell Biology/Biochemistry
Stanford University, Stanford, CA, (postdoctoral), 1993-1997, Molecular Pharmacology


Professional Experience

  • 1997-1999
    Research Scientist, Department of Molecular Pharmacology, Stanford University
  • 1999-2003
    Senior Research Scientist, Department of Molecular Pharmacology, Stanford University
  • 2003-2008
    Assistant Professor, Division of Cardiology, University of California, San Francisco
  • 2008-present
    Associate Professor, Division of Cardiology, University of California, San Francisco
  • 2008-present
    Investigator, Cardiovascular Research Institute, University of California, San Francisco

Honors & Awards

  • 1985
    President, Molecular Biology Undergraduate Society, UC Berkeley
  • 1985
    Selected graduation speaker, Department of Molecular Biology, UC Berkeley
  • 1985
    Graduated with distinction, UC Berkeley
  • 1987
    Award for Exceptional Contributions in Teaching, Department of Biological Sciences, Stanford University
  • 1988-1989
    Elected Graduate Student Representative, Dept. of Biological Sciences, Stanford University
  • 2008
    4th place winner (out of >2000), Nikon Small World Competition for microscopy

Selected Publications

  1. Overexpression of Nitric Oxide Synthase Restores Circulating Angiogenic Cell Function in Patients With Coronary Artery Disease: Implications for Autologous Cell Therapy for Myocardial Infarction. J Am Heart Assoc. 2016; 5(1).
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  2. Impairment of endothelial function by little cigar secondhand smoke. Tobacco Regulatory Science. 2016; 2(1):56-63.
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  3. Protein engineering to develop a redox insensitive endothelial nitric oxide synthase. Redox Biol. 2014 Jan 14; 2C:156-164.
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  4. Brief exposure to secondhand smoke reversibly impairs endothelial vasodilatory function. Nicotine Tob Res. 2014 May; 16(5):584-90.
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  5. Dietary flavanol intervention lowers the levels of endothelial microparticles in coronary artery disease patients. Br J Nutr. 2014 Apr 14; 111(7):1245-52.
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  6. Pleiotrophin gene therapy for peripheral ischemia: evaluation of full-length and truncated gene variants. PLoS One. 2013; 8(4):e61413.
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  7. Pharmacological inhibition of S-nitrosoglutathione reductase improves endothelial vasodilatory function in rats in vivo. J Appl Physiol (1985). 2013 Mar 15; 114(6):752-60.
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  8. Earthquake safety at work: An important topic to review with patients. San Francisco Medicine. 2012; 85(9):12-13.
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  9. Instructive nanofiber scaffolds with VEGF create a microenvironment for arteriogenesis and cardiac repair. Sci Transl Med. 2012 Aug 8; 4(146):146ra109.
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  10. Gene therapy and angiogenesis. Cardiology: An Illustrated Textbook. K. Chatterjee et al., eds. 2012; 2013-2029.
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  11. Advanced Donor Age Impairs Bone Marrow Cell Therapeutic Efficacy for Cardiac Disease. J Tissue Sci Eng. 2011 Nov 18; S3.
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  12. Blunting half of the double-edged sword: potential use of interleukin-10 to protect bone marrow-derived cells after myocardial infarction. Circ Res. 2011 Nov 11; 109(11):1196-8.
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  13. Higher fasting glucose levels are associated with reduced circulating angiogenic cell migratory capacity among healthy individuals. Am J Cardiovasc Dis. 2012; 2(1):12-9.
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  14. Donor myocardial infarction impairs the therapeutic potential of bone marrow cells by an interleukin-1-mediated inflammatory response. Sci Transl Med. 2011 Sep 14; 3(100):100ra90.
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  15. Nitric oxide counters the inhibitory effects of uremic toxin indoxyl sulfate on endothelial cells by governing ERK MAP kinase and myosin light chain activation. Biochem Biophys Res Commun. 2011 Jun 17; 409(4):758-63.
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  16. Timing of bone marrow cell therapy is more important than repeated injections after myocardial infarction. Cardiovasc Pathol. 2011; 20:204-212.
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  17. The launch of American Journal of Cardiovascular Disease. Am J Cardiovasc Dis. 2011; 1:i-ii.
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  18. Nitric oxide synthase expression and functional response to nitric oxide are both important modulators of circulating angiogenic cell response to angiogenic stimuli. Arterioscler Thromb Vasc Biol. 2010 Nov; 30(11):2212-8.
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  19. Improvement of endothelial function with dietary flavanols is associated with mobilization of circulating angiogenic cells in patients with coronary artery disease. J Am Coll Cardiol. 2010 Jul 13; 56(3):218-24.
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  20. Assessment of myocardial angiogenesis and vascularity in small animal models. Methods Mol Biol. 2010; 660:149-67.
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