Page 30 - Physico-Chemical Niche Conditions for Bone Cells

Physicochemical niche conditions and mechanosensing
Cell types of muscle (Table 1)
Table 1. Molecular markers associated with myocytes, myoblasts, and muscle stem cells Cell tpye Molecular marker(s) Reference
Myocyte MyoD(+), Myogenin(+), MHC(+), MCK(+) [26]
MuSC Myoblast
MyoD(+/-), Myf5(+/-), Pax7(+), β1-integrin(+) CXCR4(+), a7- [26–29] integrin(+), CD34(+), VCam1(+), cMet(+), Mcad(+)
MyoD(+), Myf5(+/-), Pax7(+), β1-integrin(+), CXCR4(+), a7- [26–29] integrin(+), CD34(+), VCam1(+) and fibronectin(+)
Skeletal muscle is composed of extremely long cells (i.e. myofibers) attached at both end to either tendon or bone. Myofibers are multinucleated post-mitotic cells consisting mainly of contractile filaments. In case of injury the myofiber has the ability to regenerate by activation of MuSCs, also referred to as satellite cells. MuSCs are located on top of a myofiber enclosed between the basal lamina and the plasma membrane of the myofiber (i.e. sarcolemma; Fig. 1B). Within their niche, MuSCs are anchored to the sarcolemma of the myofiber by cadherins, while on their apical side they are anchored to the basal lamina of the endomysium via integrins, syndecans, and dystroglycans [27]. Outside the basal lamina, in the interstitial space, there are fibroblasts, adipocytes, endothelial cells, fibro-adipogenic precursors, and macrophages. In intact muscle the communication between cells occurs via secretion of soluble signaling proteins. In the intact myofiber, the cells surrounding a MuSC are likely not in direct contact with this cell as this is prevented by the basal lamina. However, in an injured muscle with a ruptured basal lamina, MuSCs get into close vicinity and connect to these surrounding cells. In the beginning of muscle injury, immune cells, e.g. macrophages and monocytes, are important for regeneration after muscle injury. After immune cells are recruited, they infiltrate the muscle to get rid of necrotic tissue, and secrete soluble factors to activate MuSCs, thereby building a transient local niche condition for these cells. Then MuSCs connect to immune cells via chemokines, and immune cells help MuSCs to escape from the basal lamina of myofibers and increase MuSC proliferation [27]. In muscle injury, muscle also includes a population of fibro-adipogenic progenitors (FAPs) which are characterized by PPARγ2. Normally these cells are quiescent but they are activated upon injury. In adult tissue FAPs are the main source of adipocytes and fibroblasts, and important candidates for progenitors involved in muscle repair since there is very low homeostatic cell replacement in injured muscle. After acute damage, pro-differentiation signals (IL-6, Wnt family members, and insulin-like growth factors) may only be required in a short time, which is provided by e.g.
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