Project description:Background: BMPER, an orthologue of Drosophila melanogaster crossveinless-2, is a secreted factor that regulates BMP activity in endothelial cell precursors and during early cardiomyocyte differentiation. Although previously described in the heart, the role of Bmper in cardiac development and function remained unknown. Methods: BMPER deficient hearts were phenotyped histologically and functionally using echocardiography and Doppler analysis. Since BMPER -/- mice die perinatally, BMPER +/- mice were then challenged to pressure overload induced cardiac hypertrophy and hind limb ischemia to determine changes in angiogensis and regulation of cardiomyocyte size. Results: We identified for the first time the cardiac phenotype associated with BMPER haploinsufficiency. BMPER mRNA and protein are present in the heart during cardiac development through at least E14.5 but is lost by E18.5. BMPER +/- ventricles are thinner and less compact than sibling wild-type hearts. In the adult, BMPER +/- hearts present with decreased anterior and posterior wall thickness, decreased cardiomyocyte size, and an increase in cardiac vessel density. Despite these changes, BMPER +/- mice respond to pressure overload-induced cardiac hypertrophy challenge largely to the same extent as wild-type mice. Conclusion: BMPER appears to play a role in regulating both vessel density and cardiac development in vivo; however, BMPER haploinsufficiency does not result in marked effects on cardiac function or adaptation to pressure overload hypertrophy. Unpaired, two-condition experiment, wild-type vs BMPER+/- adult hearts. Biological replicates: 4 per condition.
Project description:Background: BMPER, an orthologue of Drosophila melanogaster crossveinless-2, is a secreted factor that regulates BMP activity in endothelial cell precursors and during early cardiomyocyte differentiation. Although previously described in the heart, the role of Bmper in cardiac development and function remained unknown. Methods: BMPER deficient hearts were phenotyped histologically and functionally using echocardiography and Doppler analysis. Since BMPER -/- mice die perinatally, BMPER +/- mice were then challenged to pressure overload induced cardiac hypertrophy and hind limb ischemia to determine changes in angiogensis and regulation of cardiomyocyte size. Results: We identified for the first time the cardiac phenotype associated with BMPER haploinsufficiency. BMPER mRNA and protein are present in the heart during cardiac development through at least E14.5 but is lost by E18.5. BMPER +/- ventricles are thinner and less compact than sibling wild-type hearts. In the adult, BMPER +/- hearts present with decreased anterior and posterior wall thickness, decreased cardiomyocyte size, and an increase in cardiac vessel density. Despite these changes, BMPER +/- mice respond to pressure overload-induced cardiac hypertrophy challenge largely to the same extent as wild-type mice. Conclusion: BMPER appears to play a role in regulating both vessel density and cardiac development in vivo; however, BMPER haploinsufficiency does not result in marked effects on cardiac function or adaptation to pressure overload hypertrophy.
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from Mus musculus tissues (Heart, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
Project description:SILAC based protein correlation profiling using size exclusion of protein complexes derived from seven Mus musculus tissues (Heart, Brain, Liver, Lung, Kidney, Skeletal Muscle, Thymus)
