Comparisons more than two groups were analyzed using one-way ANOVA

ncy between the two studies may be the difference in sample source. In the present study we isolated DNA from the whole heart that is composed of many cell types including fibroblasts, endothelial cells, smooth muscle cells and cardiomyocytes, whereas Kou et al. analyzed global DNA methylation in isolated and cultured cardiomyocytes. Nonetheless, alteration of methylation during development or aging has been noted in a variety of organs, including the heart. The present study provides novel evidence of dexamethasone-mediated premature terminal differentiation of cardiomyocytes at the critical window of heart development during early postnatal life. Dexamethasone promotes premature exit of the cell cycle and cardiomyocyte binucleation, leading to a significant decrease of proliferating cells. These effects result in a decrease in cardiomyocyte endowment in the heart. Although the present finding suggests an important role of DNA methylation in dexamethasone-mediated regulation of cardiomyocyte proliferation and binucleation in the developing heart, other mechanisms, e.g. histone modifications may not be excluded. Whereas protein methylation and DNA methylation are mediated by different mechanisms, it remains to be explored whether histone methylation is also involved in the dexamethasone-induced effects. Acknowledgments A portion of this research used the Loma Linda University School of Medicine Advanced Imaging and Microscopy Core, a facility supported in part by the National Science Foundation through the Major Research Instrumentation program of the Division of Biological Infrastructure and the Loma Linda University School of Medicine. The authors thank Dr. Christopher Wilson for providing some of the animals in the studies. 17 / 20 Dexamethasone and Heart Development ~~ ~~ Kidney allograft transplantation is the most cost-effective treatment for end stage renal PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19777101 disease. KU55933 Unfortunately, the long-term success of transplantation is often threatened by acute rejection and chronic allograft dysfunction, which are common adverse outcomes in kidney allograft recipients despite modern immunosuppression. Acute rejection occurs early post-transplant and may be antibody or T-cell mediated. Chronic allograft dysfunction is irreversible with no effective treatments. Thus, highly effective prophylactic immunosuppressive therapy is critical in preventing PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/19778700 AR and CGD. Despite the use of better immunosuppressive regimens today than 15 years ago, lymphocytes, the primary targets of immunosuppressive drugs, still find ways to evade the immune suppression. This may be due to altered genetic mechanisms and cellular pathways that lead to insufficient T and/or B-cell suppression. To address if genetic mechanisms may be related to drug related immunosuppression we investigated if gene expression changes occur before and after the start of immune suppressant therapy and over time as therapy changes. We believe that eventually gene signatures can be used to personally tailor immune suppression therapies and predict clinical outcomes. This study is the first to describe DEGs over time using whole transcriptome sequencing of PBMCs from kidney allograft recipients who have not developed AR within the first 7 months post-transplant. Previous microarray studies have focused on individuals with rejection events and have identified genes associated with AR by analyzing RNA isolated from donor kidney allograft biopsies. PBMCs have also been used to identify DEGs in kid