Satellite cells represent the stem cell population of adult skeletal muscle. The molecular mechanisms that control the proliferation of satellite cells are not well understood. In this study, we show that in response to injury, myofibres activate Wnt ligand transcription and activate a reporter cell line that is sensitive to the canonical Wnt-signalling pathway. Activated satellite cells on isolated cultured myofibres show robust expression of activated-β-catenin (Act-β-Cat), a key downstream transcriptional coactivator of canonical Wnt signalling. We provide evidence that the Wnt family of secreted glycoproteins act on satellite cells in a ligand-specific manner. Overexpression of Wnt1, Wnt3a or Wnt5a protein causes a dramatic increase in satellite-cell proliferation. By contrast, exposure of satellite cells to Wnt4 or Wnt6 diminishes this process. Moreover, we show that the prolonged satellite-cell quiescence induced by inhibitory Wnt is reversible and exposing inhibited satellite cells to stimulatory Wnt signalling restores their proliferation rate. Stimulatory Wnt proteins induce premature satellite cell BrdU incorporation as well as nuclear translocation of Act-β-Cat. Finally, we provide evidence that the Act-β-Cat translocation observed in single fibres during in vitro culture also occurs in cases of acute and chronic skeletal muscle regeneration in rodents and humans. We propose that Wnt proteins may be key factors that regulate the rate of satellite-cell proliferation on adult muscle fibres during the wound-healing response.

Microcarriers are a versatile tool with applications across a wide range of disciplines within tissue engineering. Large numbers of cells of appropriate phenotypes are required in engineering the many different tissues of the body, and microcarriers facilitate not only the expansion of many cell types but also the investigation of cell behavior in vitro. Microcarriers can also be used to directly deliver cells in vivo to repair and regenerate tissues. This review summarizes and discusses the use of microcarriers in diverse applications of tissue repair, including bone, cartilage, skin, vascular, central nervous system, adipose tissue, and liver repair. It also considers how microcarriers can be used to bulk-culture and deliver stem cells for tissue regeneration. Microcarriers thus have multidisciplinary use and advances in their use are of benefit to the entire tissue engineering field.

Galectin-1 has been implicated in the development of skeletal muscle, being maximally expressed at the time of myofiber formation. Furthermore, in the presence of exogenous galectin-1, mononuclear myoblasts show increased fusion in vitro. In the current study, we have used the galectin-1 null mouse to elucidate the role of galectin-1 in skeletal muscle development and regeneration. Myoblasts derived from the galectin-1 mutant showed a reduced ability to fuse in vitro. In galectin-1 null mutants, there was evidence of a delay in muscle fiber development at the neonatal stage and muscle fiber diameter was reduced when compared with wild-type at the adult stage. Muscle regeneration was also compromised in the galectin-1 mutant with the process being delayed and a reduced fiber size being maintained. These results, therefore, show a definitive role for galectin-1 in fusion of myoblasts both in vitro, in vivo, and in regeneration after recovery from induced injury. Developmental Dynamics 236:1014 -1024, 2007.

The aim of this study was to measure the pH on the wound surface of 30 burn patients and test the hypothesis that wound surface pH is correlated to healing time and burn depth. Inclusion criteria were any adult outpatient with burn injury. Patient age was 17 to 75 years (mean, 44), burn depth ranged from superficial to full thickness with a TBSA of 0.4 to 4%. Cause of burn included scalds, flame burn, and contact burns. On admission, and at each dressing change, the pH on the wound surface was measured. The pH in both healing and nonhealing wounds was found to decrease with each dressing change. At the second dressing change, wounds that went on to heal were found to have a significantly lower pH of 7.32 in comparison with pH 7.73 in wounds that failed to heal and therefore required subsequent grafting (P = .004). Wound pH was also correlated to depth at the second dressing change (superficial = pH 6.05, full thickness = pH 8.0). The correlation between pH and wound outcome could be used as an additional diagnostic tool to predict poor healing in wounds. Early identification of a nonhealing wound may allow a more aggressive treatment regimen, including skin grafting, to bring about rapid wound healing.