Blaxall Lab
Burns C. Blaxall, Ph.D.
Associate Professor, Department of Medicine, Aab Cardiovascular Research Institute
1999 | PhD | Pharmacology | University of Colorado Health Sciences Center
1993 | B.Sc. | Zoology and Spanish | Brigham Young University |
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Research Overview
The Blaxall lab has a long-standing interest in understanding the development, progression and regression (treatment) of heart failure. We are particularly interested in developing novel heart failure therapeutics, and are pursuing several projects with therapeutic potential, including advanced screening, medicinal chemistry, and drug development. A major focus is also to understand the pathologic intercellular communication between myocyte and non-myocyte (e.g. fibroblast) cells in the heart.
Based on 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 also pursuing several genes not previously associated in with heart failure.
Projects
Main funded projects are as follows:
- A relatively new gene, Mena, had not previously been studied in a cardiovascular context. We have now demonstrated an important functional role for Mena both in heart function and in b−AR signaling.
- Protease activated receptors (PARs), known in part for their role in blood clotting, are highly regulated in heart failure. We have demonstrated an important functional role for PARs in the pathogenesis of heart failure in the absence of blood clotting. We have also demonstrated a key role for PARs in the pathologic intercellular communication between myocytes and non-myocytes (fibroblasts) in the heart.
- Fibronectin, an important component of the extracellular matrix, plays an important role in inflammation and repair following myocardial infarction (MI). We are investigating the role of novel inhibitors of fibronectin polymerization in reducing pathologic cardiac remodeling post-MI.
- We are investigating the ability of novel small molecules to normalize b−AR – Gbg signaling and cardiac dysfunction.
- We have recently discovered a key role for mixed lineage kinases in the pathologic, intercellular communication between myocytes and fibroblasts (replicating the glia-neuron interaction in HIV-mediated neurodegeneration). We have identified small molecules targeting this pathway with therapeutic potential.
For these and other collaborative studies, we utilize a translational approach to investigate the functional cardiac and adrenergic-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 cardiac phenotyping in genetic and surgical mouse models of heart failure, coupled with validation in human cardiac myocytes and tissue samples.
Interested in learning more? Please contact: Burns_Blaxall@urmc.rochester.edu
Recent Publications
- PKC-ing Is Believing: Targeting Protein Kinase C in Heart Failure. Belmonte SL, Blaxall BC. Circ Res. 2011 Dec 9;109(12):1320-2.
- New approaches in small animal echocardiography: imaging the sounds of silence. Ram R, Mickelsen DM, Theodoropoulos C, Blaxall BC. Am J Physiol Heart Circ Physiol. 2011 Nov;301(5):H1765-80.
- S100A1: Another Step Toward Therapeutic Development for Heart Failure. Belmonte SL, Margulies KB, Blaxall BC. J Am Coll Cardiol. 2011 Aug 23;58(9):974-6.
- G protein coupled receptor kinases as therapeutic targets in cardiovascular disease.
Belmonte SL, Blaxall BC. Circ Res. 2011 Jul 22;109(3):309-19. - G protein coupled receptor kinase 2 interacting protein 1 (GIT1) is a novel regulator of mitochondrial biogenesis in heart. Pang J, Xu X, Getman MR, Shi X, Belmonte SL, Michaloski H, Mohan A, Blaxall BC, Berk BC.
J Mol Cell Cardiol. 2011 Nov;51(5):769-76.
More papers: 
Graduate Program Affiliations
Contact
Burns C. Blaxall, Ph.D.
University of Rochester
School of Medicine and Dentistry
601 Elmwood Ave, CVRI
Rochester, New York 14642
Admin. Office: (585) 276-9800
email
Lab Members
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