Project description:Mongrel dogs of either sex were randomly divided into 2 groups: 1) infection with control lentiviruses group (lenti-control, n = 6), in which control lentiviruses were injected into left superior fat pads;2) only infection with miR-206 overexpressed lentiviruses group (lenti-miR-206, n = 6), in which miR-206 lentiviruses were injected into left superior fat pads. We used microarrays to detail the global programme of mRNA expression underlying miR-206 overexpression and identified distinct classes of up-regulated and down-regulated genes during this process. Microarray-based mRNA expression profiling was performed of miR-206 overexpressed group and control group using the Affymetrix Array (CA, USA). Equal quantities of RNAs from 3 dogs were mixed to generate one sample for each experimental group.
Project description:In response to skeletal muscle injury, adult myogenic stem cells, known as satellite cells, are activated and undergo proliferation and differentiation to regenerate new muscle fibers. The skeletal muscle-specific microRNA, miR-206, is up-regulated in satellite cells following muscle injury, but its role in muscle regeneration has not been defined. Here we show that skeletal muscle regeneration in response to cardiotoxin injury is impaired in mice lacking miR-206. Loss of miR-206 also accelerates and exacerbates the dystrophic phenotype of mdx mice, a model for Duchenne muscular dystrophy. MiR-206 promotes satellite cell differentiation and fusion to form multinucleated myofibers by suppressing a collection of negative regulators of myogenesis. Our findings reveal an essential role for miR-206 in satellite cell differentiation during skeletal muscle regeneration and as a modulator of Duchenne muscular dystrophy.
Project description:In response to skeletal muscle injury, adult myogenic stem cells, known as satellite cells, are activated and undergo proliferation and differentiation to regenerate new muscle fibers. The skeletal muscle-specific microRNA, miR-206, is up-regulated in satellite cells following muscle injury, but its role in muscle regeneration has not been defined. Here we show that skeletal muscle regeneration in response to cardiotoxin injury is impaired in mice lacking miR-206. Loss of miR-206 also accelerates and exacerbates the dystrophic phenotype of mdx mice, a model for Duchenne muscular dystrophy. MiR-206 promotes satellite cell differentiation and fusion to form multinucleated myofibers by suppressing a collection of negative regulators of myogenesis. Our findings reveal an essential role for miR-206 in satellite cell differentiation during skeletal muscle regeneration and as a modulator of Duchenne muscular dystrophy. total RNA obtained from TA muscle of mdx and 3 miR-206 KO; mdx mice at 3 months of age.
Project description:Genes regulated by miR-206 were identified by microarray analysis in RD cells transfected with a Negative Control (NC) or miR-206 Mimic