Retinoic acid signalling inhibits myogenesis by blocking MYOD translation in pig skeletal muscle cells.

Vitamin A is an essential nutrient in animals, playing important roles in animal health. In the pig industry, proper supplementation of vitamin A in the feed can improve pork production performance, while deficiency or excessive intake can lead to growth retardation or disease. However, the specific molecular mechanisms through which vitamin A operates on pig skeletal muscle growth as well as muscle stem cell function remain unexplored.

Retinoic acid and RARγ maintain satellite cell quiescence through regulation of translation initiation.

In adult skeletal muscle, satellite cells are in a quiescent state, which is essential for the future activation of muscle homeostasis and regeneration. Multiple studies have investigated satellite cell proliferation and differentiation, but the molecular mechanisms that safeguard the quiescence of satellite cells remain largely unknown. In this study, we purposely activated dormant satellite cells by using various stimuli and captured the in vivo-preserved features from quiescence to activation transitions.

Disturbance of calcium homeostasis and myogenesis caused by TET2 deletion in muscle stem cells.

Skeletal muscle myogenesis is a sophisticated process controlled by genetic and epigenetic regulators. In animals, one of the key enzymes for the DNA demethylation of 5-methylcytosine is TET2. Although TET2 is essential for muscle development, the mechanisms by which TET2 regulates myogenesis, particularly the implication for muscle stem cells, remains unclear.

MicroRNA miR-509-3p inhibit metastasis and epithelial-mesenchymal transition in hepatocellular carcinoma.

Our study seeks to obtain data which help to assess the impacts and related mechanisms of microRNA miR-509-3p in hepatocellular carcinoma (HCC). We found that the expression of miR-509-3p was down-regulated and Twist was up-regulated in HCC tissues and cell lines (HepG2, HCCLM3, Bel7402, and SMMC7721) compared with the adjacent normal tissues and normal human hepatocyte (L02). Moreover, cell proliferation, invasion, migration and epithelial-mesenchymal transition (EMT) in HepG2 and HCCLM3 cells were appeared to be markedly suppressed by overexpressed miR-509-3p.

Long Non-coding RNA Regulates Porcine Satellite Cell Differentiation Through / and .

The gene promotes skeletal muscle differentiation in mice, but the regulatory models and mechanisms of myogenesis regulated by are largely unknown in pigs. Therefore, the regulatory modes of in the differentiation of porcine skeletal muscle satellite cells (PSCs) need to be determined. We observed that gene silencing could decrease the expressions of the myogenin () gene, myogenic differentiation (), and myosin heavy chain () in PSCs.

Long Noncoding Ribonucleic Acid MSTRG.59589 Promotes Porcine Skeletal Muscle Satellite Cells Differentiation by Enhancing the Function of .

Skeletal muscle satellite cells are a class of undifferentiated mononuclear myogenic stem cells distributed between the myofibroblast and membrane basement. Since their development determines the development of skeletal muscles, knowledge of their proliferation, differentiation, and fate is vital for understanding skeletal muscle development. Increasing evidence have shown that long noncoding RNA (lncRNA) plays an important role in regulating the development process of satellite cells.

Transcriptome analysis reveals long intergenic non-coding RNAs involved in skeletal muscle growth and development in pig.

Long intergenic non-coding RNAs (lincRNAs) play essential roles in numerous biological processes and are widely studied. The skeletal muscle is an important tissue that plays an essential role in individual movement ability. However, lincRNAs in pig skeletal muscles are largely undiscovered and their biological functions remain elusive.