GrnA rescues the hepatic outgrowth defect caused by miR-145 manipulation.
<p>Liver morphology was determined by EGFP expression at 4 dpf in <i>Tg (fabp10</i>:<i>EGFP)</i> embryos (A) or in embryos injected with control mimic (B), miR-145 inhibitor (C), miR-145 mimic (D), miR-145 inhibitor with <i>grnA</i> MO (0.25 ng/embryo) (E) and miR-145 mimic with <i>grnA</i> mRNA (0.4 ng/embryo) (F). Thirty embryos per experimental group were used and three independent replicates were performed. A 3D image of the liver was observed using Leica SP5 confocal microscope and Imaris software. The liver size was examined by measuring the volume of EGFP expression (G). Ten embryos per experimental group were used and three independent replicates were performed. Scale bars, 100 μm; EGFP, enhanced green fluorescent protein; *P < 0.05, t-test.</p
Biophysics, Biochemistry, Microbiology, Cell Biology, Genetics, Molecular Biology, Physiology, Developmental Biology, Cancer, Chemical Sciences not elsewhere classified, hepatic outgrowth, hepatic cell proliferation, gene expression analysis, GrnA-dependent hepatic outgrowth, miR -145 expression modulation, zebrafish hepatic outgrowth, miR -145 expression, MiR -145 mediates zebrafish hepatic outgrowth, miR -145 hairpin inhibitor, miR -145, luciferase reporter assay, miR -145 inhibitor
DOI identifier: 10.1371/journal.pone.0177887.g008
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