According to the National Institutes of Health, heart disease is the number one killer in the United States, and complications from heart disease are also very prevalent. While blockage of the coronary arteries is the most common cause of heart attacks, failure to revascularize the damaged myocardium is the most significant complication. My laboratory is investigating these two facets of coronary blood vessel function. The first area of research involves the investigation of proteins that control the growth and migration of vascular smooth muscle cells. Understanding vascular smooth muscle cells is important because overgrowth of these cells is one of the primary problems involved in restenosis. The excessive cellular growth that occurs when stents are used to open up clogged arteries.
Our second area of research is to understand the developmental processes that lead to the formation of the coronary arteries. We are interested in this area because we believe that we need to identify new mechanisms for repairing and generating new blood supplies to the cardiomyocytes to improve the outcome of heart attacks. While a significant amount of research has focused on the ability to expand or generate cardiomyocytes for replacement of the damaged tissue, less focus has been on the ability to augment the other essential component of the repair process, the blood vessel. One of the goals of my lab is to understand how these vessels form during embryonic development and then to apply this knowledge to regenerate blood vessels in a damaged heart.
RESEARCH INTERESTS
Cardiovascular development
Signal transduction
Mouse genetics
Developmental biology
Cancer biology
RECENT PUBLICATIONS
Pickett EA, Olsen GS, Tallquist MD., "Disruption of PDGFR{alpha}-initiated PI3K activation and migration of somite derivatives leads to spina bifida." Development, 3/135:589-98, February 2008
Richarte AM, Mead HB, Tallquist MD., "Cooperation between the PDGF receptors in cardiac neural crest cell migration" Developmental Biology, 306(2):785-96, April 2007
Mellgren AM, Smith CL, Olsen GS, Eskiocak B, Zhou B, Kazi MN, Ruiz FR, Pu WT, Tallquist MD., "PDGF receptor beta signaling is requiered for efficicent epicardial cell migration and development of two distinct corronary vascular smooth muscle cel populations" Circulation Research, 103 (12):1393-401, December 2008
Tallquist, MD, Soriano, P, "Cell autonomous requirement for PDGFRa in cranial and cardiac neural crest cells." Development, 130:507-518, February 2003
Wendy J. French, Esther E. Creemers, and Michelle D. Tallquist, "PDGF receptors direct vascular development independent of vascular smooth" Mol. Cell. Biol., 10.1128/MCB.00441-08 July 2008
SIGNIFICANT PUBLICATIONS
Pickett EA, Olsen GS, Tallquist MD., "Disruption of PDGFRa-initiated PI3K activation and migration of somite derivatives leads to spina bifida" Development, 3/135:589-98, February 2008
Tallquist, MD, French WJ, Soriano P., "Additive effects of PDGFRb signaling pathways in vascular smooth muscle cell development." PLoS, 1(2):E52, November 2003
Tallquist MD, Klinghoffer RA, Heuchel R, Mueting-Nelsen PF, Corrin PD, Heldin CH, Johnson RJ, Soriano P., "Retention of PDGFR-beta function in mice in the absence of phosphatidylinositol 3’-kinase and phospholipase Cgamma signaling pathways." Genes and Development., 14(24):3179-90, 2000
Tang W, Zeve D, Suh J, Bosnakovski D, Kyba M, Hammer B, Tallquist MD, Graff JM., "White fat progenitor cells reside in the adipose vasculature" Science, Epub of print Sept 18 September 2008
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