6
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Treadmill running induces satellite cell activation in diabetic mice

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Skeletal muscle-derived stem cells, termed as satellite cells, play essential roles in regeneration after muscle injury in adult skeletal muscle. Diabetes mellitus (DM), one of the most common metabolic diseases, causes impairments of satellite cell function. However, the studies of the countermeasures for the DM-induced dysfunction of satellite cells have been poor. Here, we investigated the effects of chronic running exercise on satellite cell activation in diabetic mice focused on the molecular mechanism including Notch and Wnt signaling, which are contribute to the fate determination of satellite cells. Male C57BL/6 mice 4 weeks of age were injected with streptozotocin and were randomly divided into runner group and control group. Runner group mice were performed treadmill running for 4 weeks. DM attenuated satellite cell activation and the expressions of the components of Notch and Wnt signaling. However, chronic running resulted in activation of satellite cells in diabetic mice and salvaged the inactivity of Wnt signaling but not Notch signaling. Our results suggest that chronic running induces satellite cell activation via upregulation of Wnt signaling in diabetic as well as normal mice.

          Highlights

          • Diabetes attenuates satellite cell activation.

          • Diabetes downregulates the activities of Notch and Wnt signaling.

          • Treadmill running activates satellite cells in diabetic mice.

          • Treadmill running can salvage diabetes-induced downregulation of Wnt signaling.

          Related collections

          Most cited references39

          • Record: found
          • Abstract: found
          • Article: not found

          The canonical Notch signaling pathway: unfolding the activation mechanism.

          Notch signaling regulates many aspects of metazoan development and tissue renewal. Accordingly, the misregulation or loss of Notch signaling underlies a wide range of human disorders, from developmental syndromes to adult-onset diseases and cancer. Notch signaling is remarkably robust in most tissues even though each Notch molecule is irreversibly activated by proteolysis and signals only once without amplification by secondary messenger cascades. In this Review, we highlight recent studies in Notch signaling that reveal new molecular details about the regulation of ligand-mediated receptor activation, receptor proteolysis, and target selection.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Satellite cells are essential for skeletal muscle regeneration: the cell on the edge returns centre stage.

            Following their discovery in 1961, it was speculated that satellite cells were dormant myoblasts, held in reserve until required for skeletal muscle repair. Evidence for this accumulated over the years, until the link between satellite cells and the myoblasts that appear during muscle regeneration was finally established. Subsequently, it was demonstrated that, when grafted, satellite cells could also self-renew, conferring on them the coveted status of 'stem cell'. The emergence of other cell types with myogenic potential, however, questioned the precise role of satellite cells. Here, we review recent recombination-based studies that have furthered our understanding of satellite cell biology. The clear consensus is that skeletal muscle does not regenerate without satellite cells, confirming their pivotal and non-redundant role.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Signalling downstream of activated mammalian Notch.

              Notch belongs to a family of transmembrane proteins that are widely conserved from flies to vertebrates and are thought to be involved in cell-fate decisions. In Drosophila, the Suppressor of hairless (Su(H)) gene and genes of the Enhancer of split (E(Spl)) complex, which encode proteins of the basic helix-loop-helix type have been implicated in the Notch signalling pathway. Mammalian homologues of E(Spl), such as the mouse Hairy enhancer of split (HES-1), have been isolated. Both HES-1 and the intracellular domain of murine Notch (mNotch) are able to block MyoD-induced myogenesis. Here we show that activated forms of mNotch associate with the human analogue of Su(H), KBF2/RBP-J kappa (refs 8,9) and act as transcriptional activators through the KBF2-binding sites of the HES-1 promoter.
                Bookmark

                Author and article information

                Contributors
                Journal
                Biochem Biophys Rep
                Biochem Biophys Rep
                Biochemistry and Biophysics Reports
                Elsevier
                2405-5808
                28 July 2016
                December 2016
                28 July 2016
                : 8
                : 6-13
                Affiliations
                [a ]Stem Cell Engineering Research Group, Biotechnology Research Institute for Drug Discovery, Department of Life Science and Biotechnology, National Institute of Advanced Industrial Science and Technology (AIST), Central 5, 1-1-1 Higashi, Tsukuba, Ibaraki 305-8565, Japan
                [b ]Physical Education, Health and Sport Sciences, Graduate School of Comprehensive Human Sciences, University of Tsukuba, 1-1-1 Tennodai, Tsukuba, Ibaraki 305-8574, Japan
                Author notes
                Article
                S2405-5808(16)30112-1
                10.1016/j.bbrep.2016.07.004
                5613654
                28955935
                9607aea1-8d92-4b3b-9af2-3f360d5ba831
                © 2016 The Authors

                This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

                History
                : 31 March 2016
                : 1 July 2016
                : 8 July 2016
                Categories
                Research Article

                satellite cells,diabetes,pax7,myod,wnt signaling
                satellite cells, diabetes, pax7, myod, wnt signaling

                Comments

                Comment on this article