Meeting report for Basic Cardiovascular Sciences 2011 Scientific Sessions: from concept to clinic: leading cardiovascular translational science.

The BCVS 2011 Scientific Sessions were held on July 18 to 21, 2011 in New Orleans, Louisiana. The theme of the conference for this year was “From Concept to Clinic: Leading Cardiovascular Translational Science.” The conference gathered 526 attendants, a record number for the BCVS summer conference, from 26 countries. Among them, 280 were either students or early career investigators. There were 74 oral presentations and 352 poster presentations, which were also record numbers for the past 8 BCVS meetings. The sessions were designed around the common theme of translating the most exciting and advanced basic science to further the understanding of disease pathophysiology with an eye toward novel therapeutic approaches. Here, we will briefly highlight some presentations and new features of the BCVS 2011 Scientific Sessions. The opening session was kicked off by plenary lectures given by the pioneers of several hot spots in cardiovascular research. Dr Eric Olson (University of Texas Southwestern) discussed recent advances in understanding the mechanisms of heart regeneration in mice. Dr Olson found that the regenerative activity of cardiomyocytes declines after birth when miR-195, a member of the miR-15 family, is highly upregulated. RISC RNA sequencing showed that miR-195 targets a number of cell cycle genes, including checkpoint kinase. Cardiomyocyte proliferation is upregulated when the miR-15 family is downregulated by anti-miRNAs treatment. The meeting featured an additional entire session on miRNA biology and translational science. Dr Jeffery Molkentin (Cincinnati Children’s Hospital) discussed the property of the mitochondrial permeability transition pore that regulates apoptosis and necrosis. He reported the intriguing observation that mitochondria lacking Bax/Bak do not swell but the inner mitochondrial membrane can reorganize, and permeabilization of the outer mitochondrial membrane, by any means, can restore their ability to swell and induce necrosis. Based on these observations, he proposed revised models of mitochondrial permeability transition pore, whose activity is regulated independently by the inner and outer membrane complexes. Dr Jonathan Stamler (Case Western Reserve) described his groundbreaking work in nitrosylation (S-NO) based posttranslational modification. S-NO modifications are involved in G protein coupled receptor (GPCR) signaling and in cardiac excitation contraction coupling, through dynamic influences on the ryanodine receptor. In the past decade, endogenous denitrosylases have been described by the Stamler laboratory and include S-nitrosoglutathione reductase (GSNOR) and thioredoxin. Dr Piero Anversa (Brigham and Women’s Hospital) described endogenous c-kit stem cells, and their role as adult stem cells in both the heart and the lung. Cardiac c-kit stem cells can be amplified ex vivo, have trilineage differentiation potential, and are currently being tested in clinical trials for cardiac repair. A highlight of the meeting was the keynote lecture delivered by Dr. Robert Lefkowitz (Duke University) where he discussed the role of -arrestin in mediating the signaling of the GPCR. Aside from the traditional heterotrimeric G protein signaling, GPCR mediates the mitogen-activated signaling pathway through interaction with -arrestin. Betaarrestin binds to the carboxyl terminus of the GPCR phosphorylated by G protein coupled receptor kinases. Dr Lefkowitz proposed the “Bar-code hypothesis,” in which distinct G protein coupled receptor kinase phosphorylation sites in the 2 adrenergic receptor differentially regulate -arrestin signaling, which confers an additional layer to the versatility and specificity to GPCR signaling. He showed that GPCR ligands, biased toward either -arrestin or G-protein signaling, have distinct therapeutic benefits. Beta-arrestin 2 plays an important role in mediating stabilization of -catenin in the Wnt-frizzled receptor signaling pathway in cancer stem cells. Suppression of -arrestin 2 inhibits Wnt-mediated stem cell expansion in myeloid leukemia, indicating that -arrestin 2 is a promising target in cancer therapies. In the regular sessions, 61 investigators were invited from 9 countries. The unique themes in this year’s conference included longevity and caloric restriction, microRNA and cardiovascular therapeutics, and myocyte proliferation and tissue engineering. Dr Michael Sack (NIH) presented his recent finding on the mechanism that mediates acetylation of mitochondrial proteins and its functional significance. Sirt3, a member of the sirtuin family, is activated by caloric restriction and endurance exercise and promotes protein deacetylation of mitochondrial proteins, thus enabling adaptation to aging, redox, and mechanical overload. Using bioinformatics and biochemical strategies, he has recently discovered an acetyltransferase enriched in mitochondria. He proposed that Sirt3 and the newly discovered acetyltransferase regulate the level of acetylation, thereby playing an adaptive and a The opinions expressed in News & Views are not necessarily those of the editors or of the American Heart Association. (Circ Res. 2011;109:1204-1205.) © 2011 American Heart Association, Inc.