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Altered Wnt signaling after skeletal muscle injury in CCR2-deficient mice.
Warren-GL; Hulderman-T; Liston-AL; Simeonova-PP
Appl Physiol Nutr Metab 2009 Dec; 34(6):1163
CCR2-deficient mice have impaired macrophage activities and exhibit incomplete regeneration along with fibrosis following skeletal muscle injury. The objective of this study was to determine if Wnt signaling, which is thought to play a key role in the proliferation and differentiation of muscle precursor cells, is altered in CCR2-/- mice. The tibialis anterior muscle in C57BL/6 mice, which exhibit complete regeneration after injury, and CCR2-/- mice underwent a traumatic injury. Mice were sacrificed prior to injury and at 3 and 7 days post-injury (n=5 per time point and mouse strain). RNA was isolated from injured and uninjured muscles and processed for gene expression analysis using a SuperArray Bioscience PAMM-043 qPCR array, which includes 84 genes related to Wnt-mediated signal transduction. Using a 2-way ANOVA and a Bonferroni-adjusted p value, 37 genes were found to be differentially regulated between the two strains of mice. Most of these genes (i.e., 30) were ones that in C57BL/6 mice were up-regulated at day 3 but showed decreased expression over the next 4 days. On the other hand, these genes in CCR2-/- mice exhibited increased expression from day 3 to 7. This category of genes included catenin beta-1, Dvl2, Fzd3, Fzd5, Gsk3, Sfrp1, Wnt2b, and Wnt16. Unexpectedly, no other Wnt proteins were differentially expressed between the two strains. In conclusion, the data indicate a critical role for the Wnt signaling pathway after injury in determining the completeness of recovery.
Animals; Animal-studies; Laboratory-animals; Traumatic-injuries; Proteins; Protein-biosynthesis; Genes
Issue of Publication
Applied Physiology, Nutrition, and Metabolism
Page last reviewed: September 2, 2020
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