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Molecular Cardiology Research Institute
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Lab of Vascular Myocyte Biology









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Laboratory of Vascular Myocyte Biology

Research Focus and Highlights


We are interested in how innate immunity contributes to early inflammatory events in atherosclerosis.  Smooth muscle cells constitute the primary cell type in healthy arteries, and in their normal differentiated, contractile state they regulate vascular tone and blood pressure.  These cells also have remarkable phenotypic plasticity, and under dramatic phenotypic changes, as a prelude to the disease process, including increased proliferation and synthesis of pro-inflammatory cytokines and chemokines, and extracellular matrix proteins.  Although these events begin in early childhood and precede lesion development by several decades, they set the stage for later devastating diseases such as coronary artery disease and stroke.  Our current research is using transgenic mouse models to determine how Toll-like receptors 2 and 4 contribute to phenotypic switching in smooth muscle cells, and to arterial inflammation and the accumulation of intimal lipid in the setting of hypercholesterolemia.  We are particularly interested in how SMC may regulate monocyte or T cell recruitment to lesions.


Research Administrator: Dionne Bradford

Lab Director

Debbie Beasley, Ph.D.

 

Tufts Medical Center

800 Washington Street, Box 8486

Boston, MA 02111

Debbie Beasley

   617-636-8248

  617-636-1466

Recent Publications

 

1. Role of Toll-like receptor 4 in intimal foam cell accumulation in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol.  2011 Jan.


2. Prolyl hydroxylase 2 deficiency limits proliferation of vascular smooth muscle cells by hypoxia-inducible factor-1a-dependent mechanisms. Am J Physiol Lung Cell Mol Physiol. 2009 Jun.

 

3. Simvastatin inhibits angiotensin II-Induced abdominal aortic aneurysm formation in apolipoprotein E-knockout mice. Possible role of ERK. Arterioscler Thromb Vasc Biol. 2009 Nov.

 

4. Endogenous Interleukin -1 promotes a proliferative and proinflammatory phenotype in human vascular smooth muscle cells. American Journal of Physiology - Heart and Circulatory Physiology. 2007 Feb.

 

5. Toll-like receptor 3 signaling evokes a Proinflammatory and proliferative phenotype in human vascular smooth cells. Am J Physiol Heart Circ Physiol. 2006 Jun.

 

6. Hypoxia and hypoxia-inducible factor-1alpha promote growth factor-induced proliferation of human vascular smooth muscle cells. AM J Physiol Heart Circ Physiol. 2006 Jun.

 

7. Toll-like receptor 2 mediates persistent chemokine release by Chlamydia pneumoniae-infected vascular smooth muscle cells. Arterioscler Thromb Vasc Biol. 2005 Nov.

 

8. Proinflammatory phenotype of vascular smooth muscle cells: role of efficient Toll-like receptor 4 signaling. AM J Physiol Heart Circ Physiol. 2005 Sep.

  

See All MCRI Publications