1,721,005 research outputs found
Invited Commentary on" Enrichment and Characterization of Two Subgroups of Committed Osteogenic Cells in the Mouse Endosteal Bone Marrow with Expression Levels of CD24”
No full textSkeletal muscle stem cell defects in burn-induced cachexia
Full text link..In an intriguing recent paper published in The Journal of Physiology, Fry and colleagues (Fry et al. 2016) explore the potential involvement of SCs and myonuclei apoptosis in young burn patients, a condition characterized by hyper-metabolism and extreme muscle wasting...
...The authors hypothesized that severe burn trauma could induce myonuclear apoptosis along with increased SC activation, in order to counteract the loss of myonuclei. In brief, the major findings by Fry and colleagues were (summarized in Table 1): (1) burn trauma induces myonuclear and SC apoptosis, (2) SC content is decreased although the content of active SCs is increased in burn patients, and (3) the latter two are associated with a generalized regenerative response (increased central nuclei and embMHC positive fibres) in burn patients
From innate to adaptive immune response in muscular dystrophies and skeletal muscle regeneration: the role of lymphocytes
Full text linkSkeletal muscle is able to restore contractile functionality after injury thanks to a tightly regulated process named muscle regeneration. During this process a large number of different
cells skillfully participate at muscle fibers re-building. Following muscle necrosis, debris is removed by macrophages, and Muscle Satellite Cells (MuSCs), the muscle stem cells, are activated and subsequently proliferate, migrate and fuse together to form initially small centro-nucleated fibers. These small fibers become mature after an intense protein synthesis and restore muscle functionality. Besides MuSCs, many other cell populations participate in this complex process, including interstitial non-myogenic cells. In addition, inflammatory cells also play a key role in orchestrating muscle repair. In most muscle dystrophies (MDs), MuSCs fail to properly proliferate, differentiate or replenish the stem cell compartment leading to fibrotic deposition that compromises the contractile ability of muscle.
Thus, a complete understanding of the complexity of muscle repair mechanisms and the cell
populations involved should allow the design of interventions that attenuate pathogenetic mechanisms without disrupting regenerative processes. In this review we will focus on the
contribution of immune cells in the onset and progression of MDs, with particular emphasis on Duchenne Muscular Dystrophy (DMD). In the past years, much has been learned about the crucial role of macrophages and their subtypes in MDs and healthy muscle regeneration. Much less is known about other inflammatory cells, and their eventual cross-talk, although recent observations have highlighted the role of previously under-appreciated cell populations. We will briefly summarize the current knowledge and recent advances made in our understanding of the involvement of different innate immune cells in MDs, and will move on to critically evaluate the possible role of cell populations within the acquired immune response. Revisiting previous observations in the light of recent evidence will likely change our current view of the onset and progression of the disease
Intracellular signaling in ER stress-induced autophagy in skeletal muscle cells.
No full textSkeletal muscle remodeling in response to muscle disuse and unloading is known to be associated with so-called ER stress, which, in turn, activates autophagy and contributes to muscle atrophy. Different molecules are involved in ER stress-induced autophagy, among which PKCθ has recently been described. In this study, we dissected both in vitro and in vivo ER stress-induced autophagy pathways in muscle. Using C2C12 muscle cells in culture, we demonstrated that PKC activation induced autophagy in the absence of ER stress. We further demonstrated that PKCθ was strongly activated in cultured myoblasts and myotubes during ER stress induced by different stimuli, such as TG or TN treatment, and that it localized into Lc3-positive autophagic dots upon TG treatment. Neither Akt dephosphorylation nor Foxo or GSK3β activation was observed in these conditions. Moreover, PKCθ inhibition in myoblasts and myotubes prevented ER stress-induced Lc3 activation and autophagic dot formation, but not ER stress. In vivo, lack of PKCθ prevented both food deprivation- and immobilization-induced autophagy and muscle atrophy, irrespective of Akt pathway inhibition. Taken together, these results demonstrate that PKCθ functions as an ER stress sensor in skeletal muscle, required for ER-stress-dependent autophagy activation, and can be proposed as a novel molecular target to maintain muscle homeostasis in response to external stimuli, such as disuse and unloading, still allowing intracellular clearance
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