The cellular components of the satellite cell niche participate in the regulation of skeletal muscle regeneration. Beside myogenic cells at different developmental stages, this niche is formed by cells of the immune system, the interstitial connective tissue and the vascular ystem. Unambiguous determination of the origin of these cell types could contribute to optimization of the cell-based therapy of skeletal muscle disorders. In our work, we intravenously transplanted mouse GFP+ unseparated bone marrow cells into whole-body lethally irradiated immunocom-petent mice four weeks before cardiotoxin-induced injury of the recipients’ skeletal muscles. Seven and 28 days after the toxin injection, the injured regenerating and contralateral intact muscles were examined for identification of GFP+ bone marrow-derived cells by direct fluorescence, protein immunohistochemistry and immunogold transmission electron microscopy. In both the intact and injured muscles, GFP positivity was determined in immune cells, mainly in macrophages, and in interstitial spindle-shaped cells. Moreover, in the injured muscles, rare GFP+ endothelial cells of the blood vessels and newly formed myotubes and muscle fibres were present. Our results confirmed the ability of bone marrow-derived cells to contribute to the cellular component of the satellite cell niche in the intact and regenerating skeletal muscle. These cells originated not only from haematopoietic stem cells, but obviously also from other stem or progenitor cells residing in the bone marrow, such as multipotent mesenchymal stromal cells and endothelial progenitors. and Corresponding author: Dana Čížková
The extracellular matrix (ECM) consists of proteins,
glycosaminoglycans and glycoproteins, that support the dynamic
interactions between cells, including intercellular communication,
cell attachment, cell differentiation, cell growth and migration. As
such, the ECM represents an essential and very sensitive system
within the tissue microenvironment that is involved in processes
such as tissue regeneration and carcinogenesis. The aim of the
present review is to evaluate its diversity through Ca2+ signaling
and its role in muscle cell function. Here, we discuss some
methodological approaches dissecting Ca2+ handling mechanisms
in myogenic and non-myogenic cells, e.g. the importance of Ca2+
and calpains in muscle dystrophy. We also consider the
reconstruction of skeletal muscle by colonization of decellularized
ECM with muscle-derived cells isolated from skeletal muscle.
Therefore, it is necessary to establish new methodological
procedures based on Ca2+ signaling in skeletal muscle cells and
their effect on ECM homeostasis, allowing the monitoring of
skeletal muscle reconstruction and organ repair.