TY - JOUR
T1 - Longitudinal RNA-Seq analysis of acute and chronic neurogenic skeletal muscle atrophy
AU - Ehmsen, Jeffrey T.
AU - Kawaguchi, Riki
AU - Mi, Ruifa
AU - Coppola, Giovanni
AU - Höke, Ahmet
N1 - Funding Information:
We thank the Next Generation Sequencing Core Facility at JHMI for assistance with Bioanalyzer analysis, the UCLA Neuroscience Genomics Core (UNGC) for preparing and sequencing the libraries, and Norman Barker (JHMI, Department of Pathology) for photographing Figure 1c. This work was supported by the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation (A.H. and G.C.), U.S. Department of Defense (A.H.), Maryland Stem Cell Research Fund (J.T.E.), a Burroughs Wellcome Collaborative Research Travel Grant (J.T.E.), and the National Institute of Arthritis and Musculoskeletal and Skin Diseases (J.T.E., F32AR072477). The Johns Hopkins Multiphoton Imaging Core is supported by the National Institute of Neurological Disorders and Stroke (NS050274). The myosin antibodies developed by the lab of Dr. Stefano Schiaffino were obtained from the Developmental Studies Hybridoma Bank, created by the NICHD of the NIH and maintained at the University of Iowa, Department of Biology. The content of this manuscript is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Publisher Copyright:
© 2019, The Author(s).
PY - 2019/12/1
Y1 - 2019/12/1
N2 - Skeletal muscle is a highly adaptable tissue capable of changes in size, contractility, and metabolism according to functional demands. Atrophy is a decline in mass and strength caused by pathologic loss of myofibrillar proteins, and can result from disuse, aging, or denervation caused by injury or peripheral nerve disorders. We provide a high-quality longitudinal RNA-Seq dataset of skeletal muscle from a cohort of adult C57BL/6J male mice subjected to tibial nerve denervation for 0 (baseline), 1, 3, 7, 14, 30, or 90 days. Using an unbiased genomics approach to identify gene expression changes across the entire longitudinal course of muscle atrophy affords the opportunity to (1) establish acute responses to denervation, (2) detect pathways that mediate rapid loss of muscle mass within the first week after denervation, and (3) capture the molecular phenotype of chronically atrophied muscle at a stage when it is largely resistant to recovery.
AB - Skeletal muscle is a highly adaptable tissue capable of changes in size, contractility, and metabolism according to functional demands. Atrophy is a decline in mass and strength caused by pathologic loss of myofibrillar proteins, and can result from disuse, aging, or denervation caused by injury or peripheral nerve disorders. We provide a high-quality longitudinal RNA-Seq dataset of skeletal muscle from a cohort of adult C57BL/6J male mice subjected to tibial nerve denervation for 0 (baseline), 1, 3, 7, 14, 30, or 90 days. Using an unbiased genomics approach to identify gene expression changes across the entire longitudinal course of muscle atrophy affords the opportunity to (1) establish acute responses to denervation, (2) detect pathways that mediate rapid loss of muscle mass within the first week after denervation, and (3) capture the molecular phenotype of chronically atrophied muscle at a stage when it is largely resistant to recovery.
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U2 - 10.1038/s41597-019-0185-4
DO - 10.1038/s41597-019-0185-4
M3 - Article
C2 - 31551418
AN - SCOPUS:85072602974
SN - 2052-4463
VL - 6
JO - Scientific Data
JF - Scientific Data
IS - 1
M1 - 179
ER -