Mouse Anti Bovine Myosin Heavy Chain 2A Hybridoma [TD-82]

Maternal undernutrition during gestation influences the development of the fetus, thereby increasing the risk of metabolic syndrome in adulthood. Skeletal muscle, one of the key insulin-responsive organs, is susceptible to maternal nutritional programming. This study aimed to evaluate the effect of moderate maternal energy restriction during gestation in pigs on basic events of fetal skeletal myogenesis. Primiparous, purebred Meishan sows were fed a control (normal energy intake) or a low-energy (LE) diet from mating to day 90 of gestation. Biochemical characteristics, myogenic gene expression, and myofiber characteristics were assessed in longissimus dorsi (LD) muscle of fetuses on days 55 and 90 of gestation. Fetal weights, myofiber density, and fetal umbilical vein serum triiodothyronine (T3) concentration decreased in LE group on both days 55 and 90 of gestation. The expression and activity of creatine kinase, the messenger RNA (mRNA) expression of myosin heavy chain (MYH/MyHC) genes (MYH2 and MYH4), concentration of muscular DNA and protein, and protein expression of fast-MyHC isoforms were reduced in LD muscle of LE fetuses on day 55 or 90 of gestation. Meanwhile, myogenic gene expression was reduced in LE fetuses on day 55 or 90 of gestation, indicating the downregulation of myogenesis. Additionally, the exposure to LE diet led to increased isocitrate dehydrogenase activity and slow MyHC (MYH7) mRNA expression on day 90 of gestation, suggesting the elevation of oxidative muscle metabolism. These findings suggest that moderate energy restriction during gestation attenuates fetal skeletal muscle development in pigs, resulting in the delay of skeletal muscle differentiation and maturity.

C2C12 murine myoblasts are a common model for studying muscle differentiation. Platelet endothelial aggregation receptor-1 (PEAR1), an epidermal growth factor repeat-containing transmembrane receptor, is known to participate in platelet contact-induced activation. In the present study, we demonstrated that PEAR1 is involved in the differentiation of C2C12 murine myoblasts. Western blotting and immunofluorescence staining were used to determine PEAR1 expression and localization during C2C12 cell differentiation. Subsequently, PEAR1 expression was activated and inhibited using clustered regularly interspaced short palindromic repeatsd-Cas9 technology to explore its effects on this process. PEAR1 expression was found to increase over the course of C2C12 cell differentiation. This protein was predominately localized on the membrane of these cells, where it clustered upon induction of differentiation. Expression of the myogenic markers Desmin, MYOG, and MYH2 revealed that PEAR1 positively regulated C2C12 cell differentiation. Moreover, induction of muscle injury by administration of bupivacaine to mice indicated that PEAR1 might play a role in muscle regeneration. In summary, our study confirmed the involvement of PEAR1 in C2C12 cell differentiation, contributing to our understanding of the molecular mechanisms underlying muscle development.