Project description:Transcription profiles from mice over expressing miR-154 (overExpr) were compared to profiles from mice with normal expression (control).
Project description:miR154-3p and -5p are mainly expressed in the lung epithelium pre- and postnatally in mice and are significantly higher expressed upon hyperoxia (BPD mouse model). In normoxia in vivo overexpression of miR154 (CCSPrtTA;tetOmiR154, P0-P16) leads to increased Fgf10 signaling and Tgf- signaling. Furthermore, avleolar morphometry revealed increased MLI indicating interference with alveologenesis at P16. In hyperoxia (P0-P8) in vivo overexpression of miR154 (CCSPrtTA;tetOmiR154, P0-P16) leads to decreased Fgf10 signaling and Tgf- signaling.
Project description:M. quadriceps was dissected from E18.5 mice. For transcriptome analysis, muscle tissue of wild type mice, of mice lacking both miR-1/133a genomic clusters and of mice lacking all miR-1/206/133 miRNA clusters in skeletal muscle were used.
Project description:miR-127 is an imprinted microRNA on mouse chromosome 12, strongly expressed during late embryogenesis and known regulator of placental gene Rtl1. miR-127-knockout (KO) mice appear phenotypically normal. An Illumina beadchip whole genome microarray experiment was carried out on embryonic stage 18.5 (E18.5) mice with a deletion in the miR-127 gene, and compared with wild type (WT) mice. Three tissues with varying expression of miR-127 were analysed: brain, skin and muscle.
Project description:Vertebrate lonesome kinase (VLK) is the only known secreted tyrosine kinase and responsible for the phosphorylation of a broad range of secretory pathway-resident and extracellular matrix proteins. However, its cell-type specific functions in vivo are still largely unknown. Therefore, we generated mice with a mesenchyme-specific knockout of the VLK gene (protein kinase domain containing, cytoplasmic (Pkdcc)). Most of the homozygous mice die shortly after birth, most likely as a consequence of their lung abnormalities and consequent respiratory failure. E18.5 embryonic lungs showed a reduction of alveolar type II cells, smaller bronchi, and an increased lung tissue density. Global mass spectrometry-based quantitative proteomics identified 112 proteins with significantly and at least 1.5fold differential abundance between genotypes. Twenty-five of these had been assigned to the extracellular region and 15 to the mouse matrisome. Specifically, fibromodulin and matrilin 4, which are involved in extracellular matrix organization, were significantly more abundant in lungs from Pkdcc knockout embryos. These results support a role for mesenchyme-derived VLK in lung development through regulation of matrix dynamics and the resulting non-cell-autonomous modulation of alveolar epithelial cell differentiation.