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Melatonin (N-acetyl-5-methoxy-tryptamine) is an effective antioxidant and free radical scavenger, that has important biological effects in multiple cell types and species. Melatonin research in muscle has recently gained attention, mainly focused on its role in cells or tissue repair and regeneration after injury, due to its powerful biological functions, including its antioxidant, anti-inflammation, anti-tumor and anti-cancer, circadian rhythm, and anti-apoptotic effects. However, the effect of melatonin in regulating muscle development has not been systematically summarized. In this review, we outline the latest research on the involvement of melatonin in the regulation of muscle development and regeneration in order to better understand its underlying molecular mechanisms and potential applications. [ABSTRACT FROM AUTHOR]

Skeletal muscle plays essential roles in motor function, energy, and glucose metabolism. Skeletal muscle formation occurs through a process called myogenesis, in which a crucial step is the fusion of mononucleated myoblasts to form multinucleated myofibers. The myoblast/myocyte fusion is triggered and coordinated in a muscle-specific way that is essential for muscle development and post-natal muscle regeneration. Many molecules and proteins have been found and demonstrated to have the capacity to regulate the fusion of myoblast/myocytes. Interestingly, two newly discovered muscle-specific membrane proteins, Myomaker and Myomixer (also called Myomerger and Minion), have been identified as fusogenic regulators in vertebrates. Both Myomaker and Myomixer–Myomerger–Minion have the capacity to directly control the myogenic fusion process. Here, we review and discuss the latest studies related to these two proteins, including the discovery, structure, expression pattern, functions, and regulation of Myomaker and Myomixer–Myomerger–Minion. We also emphasize and discuss the interaction between Myomaker and Myomixer–Myomerger−Minion, as well as their cooperative regulatory roles in cell–cell fusion. Moreover, we highlight the areas for exploration of Myomaker and Myomixer–Myomerger–Minion in future studies and consider their potential application to control cell fusion for cell-therapy purposes. [ABSTRACT FROM AUTHOR]

Skeletal muscles play essential roles in physiological processes, including motor function, energy hemostasis, and respiration. Skeletal muscles also have the capacity to regenerate after injury. Regeneration of skeletal muscle is an extremely complex biological process, which involves multiple cell types. Skeletal muscle stem cells (also known as satellite cells; SCs) are crucial for the development, growth, maintenance and repair of the skeletal muscle. Cell fates and function have been extensively studied in the context of skeletal muscle regeneration. In addition to SCs, other cell types, such as fibro-adipogenic precursors (FAPs), endothelial cells, fibroblasts, pericytes and certain immune cells, play important regulatory roles during skeletal muscle regeneration. In this review, we summarize and discuss the current research progress on the different cell types and their respective functions in skeletal muscle regeneration and repair. [ABSTRACT FROM AUTHOR]

In the current study, we aimed to clone the full-length cDNA of porcine CRTC3 (pCRTC3) gene and examine its expression pattern and function in intestinal epithelial cells. The full-length cDNA sequence of pCRTC3 was 2,173 bp (GenBank accession no. MF964215), with a 1,860-bp open reading frame encoding a 620-AA protein. Comparison of the deduced AA sequence with different species including human, mouse, rat, Papio, cattle, and rabbit showed 89% to 91.9% similarity. The pCRTC3 was highly expressed in small intestine and spleen, to a lesser degree in lung, liver, and adipose tissue, and was expressed at a low but detectable level in skeletal muscle, kidney, and heart. In addition, high protein levels of pCRTC3 were found in IPEC-J2 cells, in which pCRTC3 was mainly localized in cytoplasm. Furthermore, we demonstrated that knockdown of pCRTC3 significantly decreased the expression of the porcine tight junction-related genes including zonula occludens-1 (ZO-1), ZO-2, occludin, and claudin- 1 by 57.88% (P < 0.01), 40.19% (P < 0.01), 51.59% (P < 0.01), and 35.70% (P < 0.05), respectively. Taken together, we first cloned the full-length sequence of pCRTC3 and revealed the tissue-specific expression pattern, localization, and function of pCRTC3 in regulating the expression of intestinal tight junction-related genes. This study could provide some useful information for understanding the function of CRTC3 in pigs. [ABSTRACT FROM AUTHOR]

An amendment to this paper has been published and can be accessed via the original article. [ABSTRACT FROM AUTHOR]