Sandrine V. Pierre, Ph.D.


Pierre, Sandrine
Marshall Institute of Interdisciplinary Research (MIIR)
  Associate Investigator & Education Coordinator,
Adjunct Associate Professor, Joan C. Edwards School of Medicine
Department: Pharmacology, Physiology and Toxicology
Research Cluster: Cardiovascular Disease, Obesity, and Diabetes
Office: BBSC 241-N | Phone: (304) 696 – 3505
E-mail: pierres@marshall.edu

 

 

 

Live recording of aortic and ventricular pressures during ischemia and reperfusion in an ex-vivo mouse heart preparation (Langendorff).

Live recording of aortic and ventricular pressures during ischemia and reperfusion in an ex-vivo mouse heart preparation (Langendorff).


Pierre_ecg_anesthetizedmice

Research Interests

My major research interest is centered on two fundamental questions surrounding the ubiquitously expressed protein Na+,K+-ATPase: the physiological role of the Na+,K+-ATPase structural heterogeneity, and the Na+,K+-ATPase signaling function. Specifically, my laboratory’s main goal is to further characterize these new aspects of Na+,K+-ATPase structure and function and explore new ways of protecting the ischemic myocardium using the cardiac Na+,K+-ATPase as a target for therapeutic intervention.

Live recording of aortic and ventricular pressures during ischemia and reperfusion in an ex-vivo mouse heart preparation (Langendorff).

We examine these issues by combining techniques of molecular and cell biology with ex-vivo (biochemistry and cell physiology, isolated heart perfusion, primary cardiac cell cultures, histology) and in-vivo assessments of cardiac function (echocardiography, tail-cuff measurement of blood pressure, cardiac catheterization) in genetically altered mice.

Ongoing projects in the lab include:

Cardiotonic Steroids and Na+,K+-ATPase Signaling Function in cardiac ischemia and reperfusion injury

Na+,K+-ATPase is the pharmacological target of cardiotonic steroids (CS) used in the treatment of heart failure and atrial arrhythmia. The textbook explanation for CS action is the specific inhibition of Na+,K+-ATPase ion-pumping function, which is critical to their effect on Na+/Ca2+ exchange and contractility. CS also initiate intracellular signaling cascades via stimulation of the Na+,K+-ATPase signaling function. Activation of these cascades results in additional pharmacological effects of CS. A major focus of my laboratory is the exploration of one such effect, cardioprotection against cardiac ischemia/reperfusion injury, as a tool to develop novel approaches for therapeutic intervention in myocardial infarction. We believe that understanding these pathways will lead to novel interventions for the treatment and prevention of ischemia-reperfusion injury and heart failure.

Representative Publications

Physiological role of Na+,K+-ATPase structural heterogeneity

The isoform-specific region (ISR) is one of few regions of structural heterogeneity among the four isoforms of the catalytic alpha-subunit of the Na+,K+-ATPase protein complex. We use site-directed mutagenesis and heterologous expression in mammalian epithelial or cardiac cells to investigate the importance of this structural determinant for Na+,K+-ATPase isoform-specific functions and their regulation in health and diseases.

Representative Publications

Full publications, access PubMed or page on MIIR.