During heart development, cells of the primary and secondary heart field give rise to the myocardial component of the heart. The neural crest and epicardium provide the heart with a considerable amount of nonmyocardial cells that are indispensable for correct heart development. During the past 2 decades, the importance of epicardium-derived cells (EPDCs) in heart formation became increasingly clear. The epicardium is embryologically formed by the outgrowth of proepicardial cells over the naked heart tube. Following epithelial-mesenchymal transformation, EPDCs form the subepicardial mesenchyme and subsequently migrate into the myocardium, and differentiate into smooth muscle cells and fibroblasts. They contribute to the media of the coronary arteries, to the atrioventricular valves, and the fibrous heart skeleton. Furthermore, they are important for the myocardial architecture of the ventricular walls and for the induction of Purkinje fiber formation.Whereas the exact signaling cascades in EPDC migration and function still need to be elucidated, recent research has revealed several factors that are involved in EPDC migration and specialization, and in the cross-talk between EPDCs and other cells during heart development. Among these factors are the Ets transcription factors Ets-1 and Ets-2. New data obtained with lentiviral antisense constructs targeting Ets-1 and Ets-2 specifically in the epicardium indicate that both factors are independently involved in the migratory behavior of EPDCs. Ets-2 seems to be especially important for the migration of EPDCs into the myocardial wall, and to subendocardial positions in the atrioventricular cushions and the trabeculae.With respect to the clinical importance of correct EPDC development, the relation with coronary arteriogenesis has been noted well before. In this review, we also propose a role for EPDCs in cardiac looping, and emphasize their contribution to the development of the valves and myocardial architecture. Lastly, we focus on the congenital heart anomalies that might be caused primarily by an epicardial developmental defect.

The present study was designed to investigate the prevalence of swine Torque teno virus (TTV) in post-weaning multisystemic wasting syndrome (PMWS)-affected and non-affected Spanish swine. Nested PCR (nPCR) assays to detect two distinct TTV genogroups were applied. A significantly higher prevalence of TTV infection was found in sera from PMWS-affected animals (97 %) than in sera from non-PMWS-affected animals (78 %). Whilst PMWS-affected pigs (91 %) were more likely to be infected with TTV from genogroup 2 than non-PMWS-affected swine (72 %), no such difference was observed with genogroup 1. Nucleotide sequences of nPCR products were 91-99 % identical between strains within a genogroup. In contrast, inter-genogroup sequence identities were 49-58 %. Phylogenetic analyses demonstrated that genogroups form different clusters without association with PMWS or porcine circovirus type 2 infection status of the animals. These results indicate a high prevalence of both swine TTV genogroups in Spain, being present more frequently in PMWS-affected animals than in non-PMWS-affected animals.

The hSNF5 chromatin-remodeling factor is a tumor suppressor that is inactivated in malignant rhabdoid tumors (MRTs). A number of studies have shown that hSNF5 re-expression blocks MRT cell proliferation. However, the pathway through which hSNF5 acts remains unknown. To address this question, we generated MRT-derived cell lines in which restoration of hSNF5 expression leads to an accumulation in G 0 /G 1 , induces cellular senescence and increased apoptosis.

No abstract