In contrast to lower vertebrates, the mammalian heart has limited capacity to regenerate after injury in part due to ineffective reactivation of cardiomyocyte proliferation. We show that the microRNA cluster miR302-367 is important for cardiomyocyte proliferation during development and is sufficient to induce cardiomyocyte proliferation in the adult and promote cardiac regeneration. In mice, loss of miR302-367 led to decreased cardiomyocyte proliferation during development. In contrast, increase ...[more]
Project description:To define the role of miR-302-367 cluster in cardiac development, we overexpressed miR-302-367 cluster in mouse heart by using R26R-miR-302-367; Nkx2.5-Cre mice. This data set contains the microarrays examining gene expression in the hearts of R26R-miR-302-367; Nkx2.5-Cre mice at postnatal day 14. We overexpressed miR-302-367 cluster in developing mouse heart using Nkx2.5-Cre mouse line
Project description:Pluripotent marker correlation between miR-302/367-iPS, ES and fibroblast cells Mouse fibroblast were reprogrammed with miR-302/367 lentiviral vector, total RNA was extracted by trizol and microarray assay was performed
Project description:Pluripotent marker correlation between miR-302/367-iPS, ES and fibroblast cells Overall design: Mouse fibroblast were reprogrammed with miR-302/367 lentiviral vector, total RNA was extracted by trizol and microarray assay was performed
Project description:A family of vertebrate-specific microRNAs called the ESCC microRNAs regulates proliferation and differentiation of embryonic stem cells. The ESCC microRNAs arise from two genetic loci in mammals, the miR-290/miR-371 and miR-302 loci. While the miR-302 locus is found broadly among vertebrates, the miR-290/miR-371 locus is unique to eutherian species, suggesting a role in placental development. Here, we evaluate that role. A knockin reporter for the mouse miR-290 gene is expressed throughout the embryo until gastrulation, at which time it becomes specifically expressed in extraembryonic tissues and the germline. In the placenta, expression is limited to the trophoblast lineage, where it remains highly expressed until birth. Deletion of the miR-290 gene results in reduced trophoblast progenitor cell proliferation and a reduced DNA content in endoreduplicating trophoblast giant cells. A reduction in placental size precedes a reduction in fetal size and prenatal death of most knockout embryos. The vascular labyrinth shows disorganization with thickening of the barrier between maternal and fetal blood associated with reduced diffusion of a radioactive tracer. Multiple mRNA targets of the cluster miRNAs are upregulated. Together, these data uncover a critical function for the miR-290 in the regulation of a network of genes required for normal placental development, suggesting a central role for this microRNA cluster in the evolution of eutherian species. Overall design: mRNA expression in miR-290 knockout and wild-type placenta.
Project description:MEFs were infected with Oct4, Sox2, Klf4 (+/- Sall4), sorted for miR-290/302 reporter expression at day 9 (OSK) or 12 (Sall4+OSK), and then profiled. Resulting iPSCs were also profiled. Mouse ES cells were differentiated and sorted for miR-290/302 reporter expression during Fgf/Activin differentiation (day 4 or day 7). Performed in biological triplicate. Biological triplicate samples represent three independent lines. Total RNA collected with Trizol. All processing conducted at the UCLA Neuroscience Genomics Core. MouseRef-8 v2.0 Expression BeadChips.