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Expression profiles of skeletal muscle from transgenic mouse with liver specific overexpression

ABSTRACT: Expression profiles of skeletal muscle from transgenic mouse with liver specific overexpression

PROVIDER: PRJNA634327 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11825830.fastq.gz	Fastqsanger.gz
	SRR11825831.fastq.gz	Fastqsanger.gz
	SRR11825832.fastq.gz	Fastqsanger.gz
	SRR11825833.fastq.gz	Fastqsanger.gz
	SRR11825834.fastq.gz	Fastqsanger.gz

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Expression profiles of skeletal muscle from transgenic mouse with liver specific overexpression

Project description:Purpose: Next-generation sequencing (NGS) has revolutionized systems-based analysis of cellular pathways. The goals of this study are to evaluate the effects of liver-specific E4BP4 overexpression under mouse albumin promoter on the muscle glucose and lipid metabolism. Methods: We generated transgenic mice (TG) with liver-specific E4BP4 overexpression. Gasrocnemius muscles were isolated at Zeitgeber Time (ZT) 0 or 12 from transgenic mice and WT littermates, and total RNA was extracted. Muscle RNA profiles were generated by deep sequencing for four groups with three mouse samples each. Results: There were no significant differences between WT and transgenic mice at both ZT0 and 12. Conclusions: Muscle metabolism was not altered at the transcription level by liver specific overexpression of E4BP4.

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Gene expression profiling of Galgt2 overexpression in mdx skeletal muscle

Project description:Transgenic overexpression of Galgt2 in the skeletal muscles of mdx mice inhibits the development of disease pathology associated with muscular dystrophy. This is the case both in transgenic mice, where Galgt2 overexpression occurs from embryonic timepoints onward and in mdx mice where Galgt2 is overexpressed in the early postnatal period using Adeno-associated virus (AAV). Here, we use gene expression profiling to compare transcriptional changes resulting from embryonic and postnatal Galgt2 overexpression in mdx skeletal muscle. A surprising number of changes were in genes known to ameliorate muscular dystrophy when overexpressed (agrin, integrin alpha 7, ADAM12, Bcl2) or to cause muscular dystrophy when mutated (collagen VI (alpha1,alpha2), plectin 1, dystroglycan, selenoprotein N1, integrin alpha7, biglycan, dysferlin). Several genes involved in calcium homeostasis were also changed. In Galgt2 transgenic mice, where embryonic overexpression of Galgt2 in skeletal muscles alters neuromuscular development and muscle growth, the number of gene expression changes was vastly greater, however, 14% of genes altered in postnatal AAV-Galgt2 infected mdx muscles were also changed with embryonic overexpression. These experiments suggest that postnatal overexpression of Galgt2 inhibits muscular dystrophy in mdx mice via induction of a group of genes that, in aggregate, can govern membrane stability, membrane repair, calcium homeostasis, and apoptosis. Keywords: disease state analysis, gene therapy, comparative gene expression, muscular dystrophy, glycosylation, collagens, integrins, dysferlin, dystroglycan

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integrin alpha7 overexpression effects on skeletal muscle transcriptions

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Skeletal muscle specific overexpression of miRNA-1 impairs mechanical overload-induced skeletal muscle hypertrophy

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