title: Pro-inflammatory mediation of myoblast proliferation.
abstract: Skeletal muscle satellite cell function is largely dictated by the surrounding environment following injury. Immune cell infiltration dominates the extracellular space in the injured area, resulting in increased cytokine concentrations. While increased pro-inflammatory cytokine expression has been previously established in the first 3 days following injury, less is known about the time course of cytokine expression and the specific mechanisms of cytokine induced myoblast function. Therefore, the expression of IL-1β and IL-6 at several time points following injury, and their effects on myoblast proliferation, were examined. In order to do this, skeletal muscle was injured using barium chloride in mice and tissue was collected 1, 5, 10, and 28 days following injury. Mechanisms of cytokine induced proliferation were determined in cell culture using both primary and C2C12 myoblasts. It was found that there is a ∼20-fold increase in IL-1β (p≤0.05) and IL-6 (p = 0.06) expression 5 days following injury. IL-1β increased proliferation of both primary and C2C12 cells ∼25%. IL-1β stimulation also resulted in increased NF-κB activity, likely contributing to the increased proliferation. These data demonstrate for the first time that IL-1β alone can increase the mitogenic activity of primary skeletal muscle satellite cells and offer insight into the mechanisms dictating satellite cell function following injury.
authors.affiliation: Department of Kinesiology and Health, Georgia State University, Atlanta, Georgia, United States of America.
authors.forename: Jeffrey S
authors.initials: JS
authors.lastname: Otis
authors.affiliation: Medical Sciences Division, Northern Ontario School of Medicine, Thunder Bay, Ontario, Canada.
authors.forename: Sarah
authors.initials: S
authors.lastname: Niccoli
authors.affiliation: Medical Sciences Division, Northern Ontario School of Medicine, Thunder Bay, Ontario, Canada.
authors.forename: Nicole
authors.initials: N
authors.lastname: Hawdon
authors.affiliation: Medical Sciences Division, Northern Ontario School of Medicine, Thunder Bay, Ontario, Canada; Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada.
authors.forename: Jessica L
authors.initials: JL
authors.lastname: Sarvas
authors.affiliation: Department of Biomedical Sciences, Colorado State University, Fort Collins, Colorado, United States of America.
authors.forename: Melinda A
authors.initials: MA
authors.lastname: Frye
authors.affiliation: Department of Health and Exercise Science, Colorado State University, Fort Collins, Colorado, United States of America.
authors.forename: Adam J
authors.initials: AJ
authors.lastname: Chicco
authors.affiliation: Medical Sciences Division, Northern Ontario School of Medicine, Thunder Bay, Ontario, Canada; Department of Biology, Lakehead University, Thunder Bay, Ontario, Canada; Department of Health and Exercise Science, Colorado State University, Fort Collins, Colorado, United States of America.
authors.forename: Simon J
authors.initials: SJ
authors.lastname: Lees
mesh_terms: D000818:Animals; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D002478:Cells, Cultured; D053583:Interleukin-1beta / Q000494:pharmacology; D015850:Interleukin-6 / Q000494:pharmacology; D008297:Male; D051379:Mice; D032446:Myoblasts / Q000166:cytology* / Q000187:drug effects; D051381:Rats; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D053583:Interleukin-1beta; D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha