The pore sizes of the basement membranes and the extracellular matrix in the skeletal muscle are estimated at 7 nm [ 20] and 66 nm [ 19] respectively.
Just as the ECM is composed of a population of diversely functioning proteins (fibronectin, tenascins, and collagens, just to name a few), our lab has diverse projects, including mechanisms of matrix assembly, ECM in skeletal development, and metabolic effects on ECM.
Disrupted function of collagen X, a major hypertrophic cartilage matrix protein, resulted in skeletal and hematopoietic defects in endochondrally derived tissues.
Moreover, sarcoglycans are components of the dystrophin – glycoprotein complex, which link the actin cytoskeleton to the extracellular matrix in cardiac and skeletal muscle cells.
To investigate the molecular genetic basis for this delayed ossification, we cloned and examined the developmental expression of genes involved in skeletal matrix formation.
Treatment with the matrix promoted skeletal muscle regeneration in vivo and in vitro; however, the positive effects were observed only in a necrotic environment.
These molecules are very effective inhibitors of bone-matrix degradation caused by osteoclasts located in skeletal metastatic lesions [40].
The genes are involved in skeletal pattern development, bone matrix biosynthesis, osteoclast and osteoblast differentiation, calcium and phosphorus metabolism and bone related signaling pathways.
Due to its irregular pore-size and high elasticity, it seemed to be a promising matrix and has only recently been introduced in skeletal muscle tissue engineering [ 7].
Furthermore, we intended to directly compare these novel matrices with varying different consistencies and micromorphologies to established tissue engineering matrices which had not yet been applied in skeletal muscle generation.
