The aim of this study was to evaluate cell diversity by considering
how Ca2+ signaling has been adapted in skeletal muscle cell
function. We characterized single C2C12 myoblasts through
intracellular Ca2+ signaling kinetics after exposure to specific
drugs and calcium blockers using fast fluorescence
microspectrofluorimetry followed by ATP effect analysis, which
confirmed the expression of functional purinergic adenosine and
P2 receptors. Further, we found that glutamate sensitivity of
C2C12 cells was mediated by ionotropic glutamate receptors; on
the other hand, most cells were responsive to cyclopiazonic acid,
which inhibits the sarco-endoplasmic reticulum Ca2+-ATPase
pump. These results suggest that C2C12 cells possess functional
L- and P/Q-type voltage-operated Ca2+ channels, ryanodine
receptors and functional sarcoplasmic reticulum Ca2+ stores
(typical for muscle cells), adenosine and P2 purinergic receptors,
as well as ionotropic glutamate receptors. The evaluation of
intracellular Ca2+ signaling is a promising approach towards
a better understanding and control of the physiopathological
properties of myogenic cells that could be used as a predictive
factor in the selection of optimal cells for scaffold recellularization
or for tissue engineered constructs used in stem cell therapy.
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.