We have found the existence of a Bmi1+ population in the adult heart contributing to the organ low-rate turnover and repair with the generation of new cardiomyocytes. We show that the Bmi1+ population is a sub-population of the cardiac Sca-1+ progenitor cells. We have analyzed the gene profile by deep-sequencing (RNA-Seq) of Bmi1+ and Sca-1+Bmi1- cells in homeostatic heart condition. On the other hand, we have compared gene profile by deep-sequencing (RNA-Seq) of Bmi1+ cells in homeostatic condition versus Bmi1+ cells 5 days after myocardial infarction (MI). Analysis of RNA-Seq data revealed a differential expression signature between both subsets of cardiac stem/progenitors cells in homeostatic condition and also differences between Bmi1+ cells after AMI versus homeostatic condition. Overall design: Examination of gene profile of 2 different cardiac stem /progenitors subsets (Bmi1+ and Sca-1+Bmi1-) co-existing inthe adult heart under steady state. Examination of gene profile of Bmi1+ cardiac stem cells in homeostatic condition versus MI
Age-related oxidative stress confines damage-responsive Bmi1<sup>+</sup> cells to perivascular regions in the murine adult heart.
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View SamplesThe statins are a family of inhibitors of the 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase enzyme, which converts acetyl-CoA into mevalonic acid. Since HMG-CoA reductase catalyzes the rate-limiting step in the mevalonate pathway of cholesterol biosynthesis, it was thought that the major clinical benefit of statins was to reduce cholesterol levels in the bloodstream; statins are thus in wide clinical use for the prevention and treatment of cardiovascular disease. Nonetheless, mevalonate is also the precursor of isoprenoid compounds, which are substrates for the post-translational modification of many proteins involved in cell signaling. The blockade of isoprenoid synthesis might explain the pleiotropic effects described for statins in extrahepatic tissues, including inhibition of pathogen infection and anti-inflammatory and immunomodulatory activities.
A lovastatin-elicited genetic program inhibits M2 macrophage polarization and enhances T cell infiltration into spontaneous mouse mammary tumors.
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