
BSTWR 1744.1
Mailing address:
200 Lothrop Street
Pittsburgh, PA 15261
Email: sthilair@pitt.edu
Assistant:
Anna Marie Rompala amr208@pitt.edu
Other Affiliations:
Pittsburgh Heart, Lung, and Blood Vascular Medicine Institute (VMI);
Department of Bioengineering
MEMBERS
Cynthia St. Hilaire, PhD, FAHA
Assistant Professor, Department of Medicine, Division of Cardiology
University of Pittsburgh School of Medicine
Research Interests
Cardiovascular disease is the leading cause for mortality worldwide. Vascular calcification is an independent co-morbidity seen in many cardiovascular disease states and itself is a well-established marker indicative of disease severity. The overarching goal of the research conducted in the St. Hilaire Lab focuses on identifying and characterizing the mechanisms underlying the development of vascular and valvular calcification pathologies, with specific interest in defining the mechanisms by which inflammation and mechanical stress drive the transformation of a healthy vascular cell into a calcifying cell. Through collaborations with UPMC Heart and Vascular Institute surgeons Dr. St. Hilaire’s lab built a biobank of human arterial and valvular tissues and creates cell lines from healthy and diseased patients for in vitro and ex vivo studies and next-generation sequencing technologies. Using these human samples, they discovered a novel non-canonical role for telomerase in regulating the phenotypic switching of a healthy valve cell into an osteogenic calcifying cell in calcific aortic valve disease. Leveraging their experience in vascular inflammation they have embarked on a project exploring how activation of the innate immune system and signaling pathways drives transcriptional activation of osteogenic pathways and promotes endothelial cell dysfunction, ectopic calcification, and extracellular matrix remodeling. Additional ongoing projects stem from Dr. St. Hilaire’s discovery of the genetic cause of a rare disease in which patients develop non-atherosclerotic vascular calcification in their lower-extremity arteries due to mutations in the gene NT5E/CD73. Projects in this line of research aim to understand how mutations in CD73 lead to lower-extremity non-atherosclerotic vascular calcification and to define the role of CD73 and adenosine signaling in regulating extracellular matrix homeostasis and vessel tortuosity.
Technique Expertise or Resources to share
Human Tissue Biospecimen Repository
Primary Patient-specific Human Cell Lines
Murine Models
In vitro Disease Modeling
In vitro Mechanical Stretch Modeling
Keywords
Arteriosclerosis
Vascular calcification
Valvular Calcification
Calcific Aortic Valve Disease
Vascular Remodeling
Vascular Disease Pathogenesis
Innate Immunity Signaling
Laboratory
Lab website: http://www.sthilairelab.pitt.edu/
Lab Members
Rolando Cuevas, PhD | Postdoctoral Fellow |
Michael Bashline, MD | Cardiology Fellow |
Billy Moorhead, BS | Research Technician |
Claire Chu, BS | Research Technician |
Ryan Wong, BS | Research Technician |
Angela Le | Undergraduate Researcher |
Alex Crane | Undergraduate Researcher |