Sandrine V. Pierre, PhD
Associate Investigator & Education Coordinator
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.