Benjamin Prosser, PhD

Assistant Professor

Lab Web Site

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726 Clinical Research Building

415 Curie Boulevard

Philadelphia, PA 19104

215-746-1488

bpros@pennmedicine.upenn.edu

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Diastolic stretch triggers detrimental calcium signaling in heart cells from mice with muscular dystrophy.

Benjamin Prosser, PhD


Assistant Professor of Physiology

Other Perelman School of Medicine Affiliations


Degrees & Education

  • BS, Wake Forest University, 2005

  • PhD, University of Maryland School of Medicine, 2009


Awards & Honors

  • 2011 Outstanding Postdoctoral Scholar Award


Professional Affiliations

  • Biophysical Society

  • Cardiac Muscle Society

  • Penn Center for Musculoskeletal Diseases


Research Description

With each heartbeat, the mechanical stress of cardiomyocyte contraction and relaxation is converted into intracellular signals through a process termed “mechanotransduction”. While critical for the hearts normal, adaptive response to stress, faulty stress-sensing is intimately linked to heart disease. Despite this importance in human health, the cellular and molecular mechanisms of mechanotransduction remain poorly understood. The goal of our lab is to unravel these mechanisms; we combine novel techniques to manipulate mechanical stress at the single cell level with high-speed and super-resolution imaging to evaluate sub-cellular responses to mechanical stimuli with unprecedented spatial and temporal resolution.

The lab is currently focused on how cell stress and strain regulate intracellular calcium homeostasis and signaling through reactive oxygen species (ROS). When a heart cell is stretched, as occurs during diastolic filling of the ventricles with blood, ROS are generated and modulate the activity of intracellular calcium release channels. This mechano-signaling requires a stable microtubule network and the ROS-producing enzyme NADPH-oxidase, but the details of these interactions remain to be determined. The stretch-dependent burst of ROS serves to enhance cardiac excitation-contraction coupling in healthy cells, but may trigger calcium-dependent arrhythmias under disease conditions. We are actively investigating the molecular mechanisms underlying this and similar mechanotransduction pathways, and how they affect normal and pathological ROS and calcium signaling in the heart and other tissues.


Click here for a full list of publications.
(searches the National Library of Medicine's PubMed database.)


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