Meeting Review: Cardiomyocyte Regeneration and Protection, La Jolla, California, June 2011

Abstract

The concept of an Abcam-supported meeting on a specific topic panned out very well in La Jolla in June 2011. Cosponsored by the International Society for Translational Cardiovascular Research, the program provided a near optimal interaction between basic science in the stem cell field as well as attention to recently completed and ongoing clinical trials. It was a true translational cardiovascular meeting on the potential application of cells for therapy. In addition, there was a mix of senior and junior scientists in each session, with a number of speakers selected based upon the abstracts submitted. The meeting opened by brief comments by Mark Mercola on behalf of the organizers, which also included Nabil Dib and Pieter A. Doevendans. The first session on cellular replacement started with an excellent presentation by Bernd Fleishmann (Bonn, Germany), who addressed various topics related to cardiac repair, optical induction of cellular depolarization, and contraction, ending with control of cardiomyocyte cell cycle. Connexin 43 expression appears to be crucial to reduce the arrhythmic substrate post myocardial infarction (MI) in rodent models. Various interventions—stem cells overexpressing CX 43, transgenic models, and gene therapy—led to the conclusion that increasing Cx43 levels is cardioprotective. In the discussion that followed, it appeared that transplantation of mesenchymal stem cells overexpressing Cx43 might be an effective means to preserve myocardial function post-MI. The general concept is that improved cell–cell interaction and conduction have a protective effect on cell survival and protects against arrhythmias, and more work is warranted to establish the underlying mechanism. Another biologically fascinating approach was to overexpress channel rhodopsin, a single-component, lightactivated cation channel originally isolated from algae, to make the cells depolarize in response to light pulses. Contraction as well as pacemaker activity could be induced. Dr. Fleishmann then focused on the use of anillin to identify dividing cells. Anillin is a nuclear protein, involved in the regulation of cytokinesis. By localizing to the bridge connecting two daughter cells, an eGFP–anillin fusion protein allows tracing of dividing cells and the visualization of the induction of cell cycle under pathological conditions, overall a beautiful work and a dynamic presentation. Andreas Zeiher (Frankfurt, Germany) needs little introduction. He discussed the current position of cell therapy in clinical practice. Although the direct and long-term benefit of cell therapy after MI is modest, there is an effect on prognosis. Mechanistically, the current therapies aim to improve the local milieu after MI and induce angiogenesis through paracrine factors. The effects were especially significant in patients with extensive damage (EF <40%, n=20), accounting for most of the benefit in clinical trials. Potential mechanisms involved were addressed the next day by Stefanie Dimmeler. A new study focusing on large MI and clinical endpoints like mortality was recently approved by the EU for funding and will start later in 2011. The study will use bone marrow-derived mononuclear cells that will be injected intracoronary. This study will be crucial to determine the application of stem cell treatment post-MI in routine clinical practice. More recently, the focus of cell therapy has shifted to patients in cardiac failure. M. Mercola (*) Muscle Development and Regeneration Program, Sanford-Burnham Medical Research Institute, La Jolla, San Diego, CA, USA e-mail: mmercola@burnham.org