Sixteen castrated male Large White × Landrace pigs were employed to investigate the muscle type-specific changes of gene expression in response to recombinant porcine growth hormone (rpGH) administration. Pigs were injected intramuscularly with rpGH (4 mg/day, n = 8) or saline (n = 8) for 28 days. Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to determine the mRNA abundance of genes related to muscle growth in longissimus dorsi (LD) and semitendinosus (ST) muscles. Myofibre-type composition was characterised by the ratio of the expression of myosin heavy chain (MyHC) 1, 2a or 2b relative to 2x. The results showed that the relative myofibre-type composition of neither LD nor ST was affected by rpGH administration. rpGH administration did not induce significant changes in the abundances of myostatin and myogenin mRNA in both types of muscle. MyoD and calpain 3 mRNA were significantly increased after rpGH treatment in ST muscle, whereas the difference was not significant in LD muscle. A tendency of down-regulation was observed for PGC-1α mRNA expression in ST muscle of rpGH-treated group (P = 0.16). These results suggest that myoD, calpain 3 and probably PGC-1α may be involved in the mechanism of exogenous GH action on skeletal muscle growth; rpGH up-regulates mRNA expression of myoD and calpain 3 in a muscle type-specific manner, being more remarkable in ST than in LD, whereas no influences of rpGH on the mRNA expression of myostatin and myogenin were detected.

Infection of an intracellular parasitic nematode, Trichinella spiralis, resulted in severe damage in muscle cells which was followed by activation and proliferation of satellite cells. The repairing process, shortly after the damage, histopathologically resembled those seen after mechanical injury. Resemblance was also true for kinetics of expression of myogenic regulatory factors (MyoD, myogenin and MRF4). The difference resided in the next step where the muscle cell infected with T. spiralis transformed to a unique cell which is parasitologically known as the nurse cell, and the proliferated satellite cells did not differentiate to the muscle cell but to the nurse cell (misdifferentiation). Thus the nurse cell was a fusion of the transformed infected muscle cell and misdifferentiated satellite cells. Infection with another species of Trichinella, T. pseudospiralis, also caused cell damage, but more extensively involving the entire length of the infected muscle cells because no septum was formed to minimize the affected area. Therefore, a large number of satellite cells were activated and proliferated. The myogenic regulatory factors such as MyoD and myogenin were activated for a longer period than in the case with T. spiralis infection. The infected muscle cell transformed to the nurse cell, whose cytoplasm was characterized by extensive smooth endoplasmic reticulum. Satellite cells misdifferentiated to the nurse cell, whose cytoplasm was amorphous, void of distinct cell organelles. The two kinds of cytoplasm did not fuse as examined thus far. Thus infection with T. spiralis and T. pseudospiralis caused misdifferentiation of satellite cells, but in a different way.

The identification of myogenic precursor cells (mpc) is a key factor in determining the early events in the myogenesis and regeneration of skeletal muscle. Although satellite cells have long been established as the providers of myoblastic cells, very little is really known (apart from their anatomical location in relation to muscle fibres and their ability to migrate) about the precise role of satellite cells in myogenesis. Numerous techniques for labelling mpc have been devised, but none of these has proven to be completely reliable in firmly establishing the origin of myogenic cells. The use of tritiated thymidine to label DNA in proliferating mpc (which are not specifically distinguishable at the time) and the subsequent location of their labelled progeny in myotube nuclei has revealed a great deal of data on the timing of myogenesis, but not about the nature of mpc themselves. DNA synthesis can also be detected by antibodies to the thymidine analogue, bromodeoxyuridine, and also by antibody staining for proliferating nuclear cell antigen. Like tritiated thymidine, these other markers are not specific for muscle but are general markers for DNA synthesis. In situ hybridisation of various muscle-specific genetic markers and their products has been informative, as has immunolabelling of myogenin, MyoD1 and desmin. Desmin labelling has been particularly instructive in identifying mpc because it is one of the first muscle-specific proteins to be produced in mpc. This review covers some of the techniques mentioned above and their usefulness in determining the early events in myogenesis.