In my lab, we are interested in the development of blood vessels. Certain diseases require blood vessel development for their progression; tumors, for example, thrive on blood flow. In those situations, we want to know how to stop vessel growth in order to stop disease progression. At other times, such as when wounds are healing, vessel growth is necessary and positive. In those cases we want to learn how to build new vessels.
Blood vessel development is similar in mice and humans, so we use mice to study and manipulate vessels. Much of our work is carried out in mouse embryos, since they undergo rapid and easily visible blood vessel development.
Because we want to understand what genes are required for blood vessel development, we study certain enzymes that help turn genes on and off. These enzymes are specifically involved in relaxing DNA that is normally tightly coiled up in our cells. When DNA is relaxed, genes can be regulated. We use genetically engineered mice to shut down these enzymes that relax DNA in order to determine the effect on blood vessel development. We ultimately hope to identify the particular genes that these enzymes regulate during vascular development, since those genes would be important therapeutic targets for controlling the process of vessel growth.
My lab studies the transcriptional regulation of genes that impact blood and lymphatic vascular development and maintenance. I became interested in vascular biology and development during my graduate training with Shaun Coughlin at UCSF and in epigenetics and transcription during my postdoctoral training with Terry Magnuson at UNC-Chapel Hill. When I launched my independent career in the Cardiovascular Biology Research Program at OMRF in 2008, I combined these interests together and initiated a program studying the impact of ATP-dependent chromatin-remodeling complexes on vascular development. These complexes transiently modulate chromatin to facilitate transcriptional regulation of target genes. By generating mice with vascular-specific mutations in these complexes, my lab assesses how chromatin remodeling influences expression of genes that affect endothelial cell morphology and behavior. Our long-term goal is to generate insights that can be exploited for developing therapeutic approaches to combat vascular pathologies.
For more details about our current research, please see my lab website: https://griffinc.omrf.org/
B.A., Harvard University, Cambridge, MA, 1995
Ph.D., University of California, San Francisco, CA, 2001
Postdoc, University of North Carolina at Chapel Hill, 2001-2008
Honors and Awards
1995 Magna cum laude with highest honors in Biology, Harvard College
1998-2001 American Heart Association Predoctoral Fellowship
2002-2005 National Research Service Award Postdoctoral Fellowship
2005-2006 American Heart Association Postdoctoral Fellowship
2006-2011 NIH Pathway to Independence Award
2011 TEDxOU: Epigenetics and the Influence of Our Genes
2013 J. Donald and Patricia Capra Award for Scientific Achievement
2009-present: Ad hoc peer review for AHA (SouthWest Affiliate and National) and for NIH (CDD and VCMB study sections)
2014-present: AHA SouthWest Affiliate Research Committee Member
2015-2018: NAVBO Councilor
2016-present: Editorial Board Member for Angiogenesis
North American Vascular Biology Organization
Society for Developmental Biology
American Heart Association
Joined OMRF Scientific Staff in 2008
Ungvari Z, Tarantini S, Kiss T, Wren JD, Giles CB, Griffin CT, Murfee WL, Pacher P, Csiszar A. Endothelial dysfunction and angiogenesis impairment in the ageing vasculature. Nat Rev Cardiol. 2018 May 24. Review. PMID: 29795441
Gao S, Silasi-Mansat R, Behar M, Lupu F, Griffin CT. Excessive plasmin compromises hepatic sinusoidal vascular integrity after acetaminophen overdose. Hepatology. 2018 May 5. PMID: 29729197
Menendez MT, Ong EC, Shepherd BT, Muthukumar V, Silasi-Mansat R, Lupu F, Griffin CT. BRG1 (Brahma-Related Gene 1) Promotes Endothelial Mrtf Transcription to Establish Embryonic Capillary Integrity. Arterioscler Thromb Vasc Biol. 2017 Jul 20. pii: ATVBAHA.117.309785. [Epub ahead of print] PMID: 28729363
Liu X, Pasula S, Song H,... Griffin C, Xia L, Srinivasan RS, Chen H. Temporal and spatial regulation of epsin abundance and VEGFR3 signaling are required for lymphatic valve formation and function. Sci Signal. 2014 Oct 14;7(347):ra97. PMCID:PMC4226761
Chen H, Griffin C, Xia L, Sathish SR. Molecular and cellular mechanisms of lymphatic vascular maturation. Microvasc Res. 2014 Nov;96:16-22. PMCID:PMC4263685
Ingram KG, Curtis CD, Silasi-Mansat R, Lupu F, Griffin CT. The NuRD Chromatin-Remodeling Enzyme CHD4 Promotes Embryonic Vascular Integrity by Transcriptionally Regulating Extracellular Matrix Proteolysis. PLoS Genet. 2013;9(12):e1004031. PMCID:PMC3861115
Davis RB, Curtis CD, Griffin CT. BRG1 promotes COUP-TFII expression and venous specification during embryonic vascular development. Development. 2013 Mar;140(6):1272-81. PMCID:PMC3585661
Curtis CD, Griffin CT. The chromatin-remodeling enzymes BRG1 and CHD4 antagonistically regulate vascular Wnt signaling. Mol Cell Biol. 32:1312-1320, 2012. [Abstract]
Cardiovascular Biology Research Program, MS 45
Oklahoma Medical Research Foundation
825 N.E. 13th Street
Oklahoma City, OK 73104
Phone: (405) 271-7073
Fax: (405) 271-7417
Matthew Menendez, Ph.D.
Chris Schafer, Ph.D.
Jun Xie, M.D.
Research Trainee (Polish Student Exchange Program)
Administrative Assistant II