We are analyzing https://link.springer.com/article/10.1007/s00418-012-1018-0.

Title:
An anti-inflammatory role for leukemia inhibitory factor receptor signaling in regenerating skeletal muscle | Histochemistry and Cell Biology
Description:
Skeletal muscle regeneration in pathology and following injury requires the coordinated actions of inflammatory cells and myogenic cells to remove damaged tissue and rebuild syncytial muscle cells, respectively. Following contusion injury to muscle, the cytokine leukemia inhibitor factor (LIF) is up-regulated and knockout of Lif negatively impacts on morphometric parameters of muscle regeneration. Although it was speculated that LIF regulates muscle regeneration through direct effects on myogenic cells, the inflammatory effects of LIF have not been examined in regenerating skeletal muscle. Therefore, the expression and function of LIF was examined using the antagonist MH35-BD during specific inflammatory and myogenic stages of notexin-induced muscle regeneration in mice. LIF protein and mRNA were up-regulated in two distinct phases following intramuscular injection of notexin into tibialis anterior muscles. The first phase of LIF up-regulation coincided with the increased expression of pro-inflammatory cytokines; the second phase coincided with myogenic differentiation and formation of new myotubes. Administration of the LIF receptor antagonist MH35-BD during the second phase of LIF up-regulation had no significant effects on transcript expression of genes required for myogenic differentiation or associated with inflammation; there were no significant differences in morphometric parameters of the regenerating muscle. Conversely, when MH35-BD was administered during the acute inflammatory phase, increased gene transcripts for the pro-inflammatory cytokines Tnf (Tumor necrosis factor), Il1b (Interleukin-1β) and Il6 (Interleukin-6) alongside an increase in the number of Ly6G positive neutrophils infiltrating the muscle were observed. This was followed by a reduction in Myog (Myogenin) mRNA, which is required for myogenic differentiation, and the subsequent number of myotubes formed was significantly decreased in MH35-BD-treated groups compared to sham. Thus, antagonism of the LIF receptor during the inflammatory phase of skeletal muscle regeneration appeared to induce an inflammatory response that inhibited subsequent myotube formation. We propose that the predominant role of LIF in skeletal muscle regeneration appears to be in regulating the inflammatory response rather than directly effecting myogenic cells.
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article, google, scholar, cas, pubmed, factor, muscle, inhibitory, leukemia, lif, skeletal, cell, cells, regeneration, receptor, differentiation, physiol, inflammatory, myogenic, white, expression, mhbd, biol, murine, res, role, regenerating, injury, mice, administration, necrosis, growth, leukaemia, austin, sci, nicola, data, hunt, jazayeri, effects, mrna, phase, cytokines, muscular, dystrophy, myoblast, metcalf, mast, fig, day,

Topics {✒️}

mh35-bd-treated groups compared month download article/chapter real-time rt-pcr post-natal skeletal muscle bestkeeper–excel-based tool stem cell factor rest comparing mh35-bd leukaemia inhibitory factor notexin-induced muscle regeneration tumor necrosis factor leukemia inhibitory factor phosphotidylinositol 3-kinase-mediated inhibition muscular dystrophy association full article pdf mdx muscular dystrophy pro-inflammatory cytokines tnf skeletal muscle cells skeletal muscle growth skeletal muscle regeneration immune system il-1 beta accumulation privacy choices/manage cookies regenerating skeletal muscle stem cells 17 notexin-induced regeneration anti-lif blocking peptide activated mast cells mature mast cells ciliary neurotrophic factor antagonist mh35-bd muscular dystrophy physiol-cell physiol 292 physiol-cell physiol 285 rat gastrocnemius muscle related subjects de souza dp c-myc signalling dystrophin-deficient muscle spencer mj pro-inflammatory cytokines therapeutic lif transgene tibialis anterior muscles il-6 signal transducer human adrenal cortex article histochemistry cell biology aims cell cycle inhibitors corticotroph cell line mh35-bd administration myoblast cell number

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         description:Skeletal muscle regeneration in pathology and following injury requires the coordinated actions of inflammatory cells and myogenic cells to remove damaged tissue and rebuild syncytial muscle cells, respectively. Following contusion injury to muscle, the cytokine leukemia inhibitor factor (LIF) is up-regulated and knockout of Lif negatively impacts on morphometric parameters of muscle regeneration. Although it was speculated that LIF regulates muscle regeneration through direct effects on myogenic cells, the inflammatory effects of LIF have not been examined in regenerating skeletal muscle. Therefore, the expression and function of LIF was examined using the antagonist MH35-BD during specific inflammatory and myogenic stages of notexin-induced muscle regeneration in mice. LIF protein and mRNA were up-regulated in two distinct phases following intramuscular injection of notexin into tibialis anterior muscles. The first phase of LIF up-regulation coincided with the increased expression of pro-inflammatory cytokines; the second phase coincided with myogenic differentiation and formation of new myotubes. Administration of the LIF receptor antagonist MH35-BD during the second phase of LIF up-regulation had no significant effects on transcript expression of genes required for myogenic differentiation or associated with inflammation; there were no significant differences in morphometric parameters of the regenerating muscle. Conversely, when MH35-BD was administered during the acute inflammatory phase, increased gene transcripts for the pro-inflammatory cytokines Tnf (Tumor necrosis factor), Il1b (Interleukin-1β) and Il6 (Interleukin-6) alongside an increase in the number of Ly6G positive neutrophils infiltrating the muscle were observed. This was followed by a reduction in Myog (Myogenin) mRNA, which is required for myogenic differentiation, and the subsequent number of myotubes formed was significantly decreased in MH35-BD-treated groups compared to sham. Thus, antagonism of the LIF receptor during the inflammatory phase of skeletal muscle regeneration appeared to induce an inflammatory response that inhibited subsequent myotube formation. We propose that the predominant role of LIF in skeletal muscle regeneration appears to be in regulating the inflammatory response rather than directly effecting myogenic cells.
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