Burns C. Blaxall, Ph.D.

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Contact

University of Rochester
School of Medicine and Dentistry
601 Elmwood Ave, ACVRI - 211 Bailey Road
Rochester, New York 14642

Office: 585 276-9791 (primary)

Lab: 585 276-9850

Fax: 585 276-9830

Portrait

My laboratory has a long-standing interest in understanding the development, progression and regression (treatment) of heart failure, particularly as it relates to beta-adrenergic receptor (beta-AR) signaling. We have recently identified differential expression of a number of novel genes associated with both the development and regression of cardiac disease by large-scale gene expression profiling of both mouse and human heart tissue from non-failing, failing, and genetically or surgically "rescued" cardiac phenotypes. We are pursuing three main projects based largely on genes identified in these studies:

1) A relatively new gene, named Mena, had not previously been studied in a cardiovascular context. Prior to our studies, Mena was known to be a cytoarchitectural gene that played a role in cell/neuron/axon migration. We have demonstrated an important functional role for Mena in cardiac structure, function and beta-AR signaling.

2) Protease activated receptors (PARs), known in part for their role in blood clotting, were also found to be highly regulated in heart failure. We have demonstrated an important functional role for PAR expression and activity in cardiac cells in the pathogenesis of heart failure.

3) Finally, beta-ARs are chronically desensitized and downregulated in heart failure. We are investigating the ability of novel small molecules to normalize pathologic b-AR signaling and cardiac dysfunction.

For these and other collaborative studies, we utilize a translational approach to investigate the functional cardiac and beta-AR-related relevance of specific genes and molecules. Our investigational techniques range from in vitro biochemistry, pharmacology, cell biology and isolated adult cardiomyocyte contractility studies to high-resolution in vivo c rdiac phenotyping in genetic and surgical mouse models of heart failure, coupled with validation in human heart failure cardiac myocytes and tissue samples.

Interested in learning more? Please contact: Burns_Blaxall@urmc.rochester.edu

Current Appointments

Education
B.Sc. Zoology and Spanish Brigham Young University 1993
PhD Pharmacology University of Colorado Health Sciences Center 1999
Post-Doctoral Training & Residency
Postdoctoral Fellow Walter J, Koch, Ph.D., Department of Surgery Duke University Medical Center Durham, NC 27710 1999 - 2003
Fellowship Awards
Postdoctoral Fellowship (Top-Ranked Fellowship Award) American Heart Association 2000 - 2002
Advanced Predoctoral Fellowship in Pharmacology Pharmaceutical Research and Manufactures Associates of America Foundation 1997 - 1999
NIH Pre-Doctoral Training Grant Appointment (GM07635) 1993 - 1996

Lab Description

Our laboratory has a long-standing interest in the development, progression and regression (treatment) of heart failure, particularly as it relates to b(beta)-adrenergic receptor (b-AR) signaling.


Lab Website

http://www.urmc.rochester.edu/cvri/research/blaxall-lab.cfm


Recent Journal Articles
Showing the 5 most recent journal articles. (34 available)
Bullard TA; Protack TL; Aguilar F; Bagwe S; Massey HT; Blaxall BC. "Identification of Nogo as a novel indicator of heart failure". Physiolog Genom 32 (2008): 182-9.
Blaxall BC. "Personalized Medicine: Are we there yet?". J Cardiovasc Transl Res (2008).
Ashley EA: Blaxall BC. "A GINA (Genetic Information Non-Discrimination Act) Primer". J Cardiovasc Transl Res (2008).
Zhu, M.; Reiken, S.; Liu, G.; Xu, X.; Gehrmann, J.; Zhang, J.; Mao, L.; Rockman, HA.; Berul, CI.; Koren, G.; Marks, AI.; Blaxall, BC.; Mende, U. ". Enhanced Calcium Cycling and Contractile Function in Transgenic Hearts Expressing Constitutively Active G?o Protein." Amer J Physiol Heart Circ Physiol, 294 (2008): H1335-H1347.
Satoh, K.; Nigro, P.; O'Dell, MR.; Cui, Z.; Liao, DF.; Menon, P.; Mohan, A.; Abe, J.; Yan, C.; Blaxall, BC.; Berk, BC. "Cyclophilin A is required for angiotensin II-induced cardiac hypertrophy." Circulation (2008).