Diabetes and many other metabolism syndromes are closely related to obesity. To reveal the underlying mechanism of fat deposition, an increasing number of studies are focusing on the functions of miRNAs during adipocytes development. Previous studies have proved that miR-15a/b play important roles in multiple physiological processes; however, their functions during adipogenesis remain unclear. To reveal this, we detected the expression profiles of miR-15a/b during adipogenesis in porcine pre-adipocyte, and found that their expression levels increased in the early stage of adipocyte differentiation and dropped after day 4. Moreover, over-expression of miR-15a/b in porcine pre-adipocytes promoted adipocyte differentiation and lipid accumulation. Target genes of miR-15a/b were predicted and examined, which revealed that Forkhead box protein O1 (FoxO1) is the target gene of miR-15a/b. The inhibition of FoxO1 expression level caused by miR-15a/b over-expression had a positive effect on adipogenesis. Thus, we conclude that miR-15a/b promote adipogenesis in porcine pre-adipocyte via repressing FoxO1.

Bone morphogenic protein and activin membrane-bound inhibitor (BAMBI) is regarded as an essential regulator of cell proliferation and differentiation that represses transforming growth factor-β and enhances Wnt/β-catenin signaling in various cell types. However, its role in skeletal muscle remains largely unknown. In the current study, we found that the expression level of BAMBI peaked in the early differentiation phase of the C2C12 rodent myoblast cell line. Knockdown of BAMBI via siRNA inhibited C2C12 differentiation, indicated by repressed MyoD, MyoG, and MyHC expression as well as reductions in the differentiation and fusion indices. BAMBI knockdown reduced the activity of Wnt/β-catenin signaling, as characterized by the decreased nuclear translocation of β-catenin and the lowered transcription of Axin2, which is a well-documented target gene of the Wnt/β-catenin signaling pathway. Furthermore, treatment with LiCl, an activator of Wnt/β-catenin signaling, rescued the reduction in C2C12 differentiation caused by BAMBI siRNA. Taken together, our data suggest that BAMBI is required for normal C2C12 differentiation, and that its role in myogenesis is mediated by the Wnt/β-catenin pathway.

The microRNA (miR)-17 family is widely expressed in mammalian tissues and play important roles in various physiological and pathological processes. Here, the functions of miR-106a-5p, a member of miR-17 family, were explored during myogenic differentiation in C2C12 cell line. First, miR-106a-5p was found to be relatively lower expressed in two-month skeletal muscle tissues and gradually decreased upon myogenic stimuli. Forced expression of miR-106a-5p significantly reduced the differentiation index, fusion index as well as the expression of myogenic markers (MyoD, MyoG, MyHC, Myomixer, Myomarker). Meanwhile, the levels of phosphorylated AKT were reduced by overexpression of miR-106a-5p, and administration of insulin-like growth factor 1 (IGF1), a booster of myogenic differentiation, could recover all the inhibitory effects above of miR-106a-5p. Furthermore, miR-106a-5p was elevated in aged muscles and dexamethasone (DEX)-treated myotubes, and up-regulation of miR-106a-5p significantly reduced the diameters of myotubes accompanied with increased levels of muscular atrophy genes and decreased PI3K/AKT activities. Finally, miR-106a-5p was demonstrated to directly bind to the 3’-UTR of PIK3R1, thus, repress the PI3K/AKT signaling.

Sirtuins are Class III histone deacetylases (HDACs) that have emerged as important regulators of diverse biological processes, and comprised of seven members (Sirt1 to Sirt7) [1]. Sirt2 predominantly resides in the cytoplasm, deacetylates lysine40 on α-tubulin, and co-localizes with microtubules and HDAC6 [2]. Sirt2 plays an important role in the control of mitotic exit in cell cycle, and the increased Sirt2 activity severely delays cell cycle progression through mitosis [3–5]. Sirt2 is hyper-phosphorylated and accumulated in the M phase, which regulates mitotic progression [3]. In glioblastoma cancer stem cells, sphere-forming capacity and cell proliferation are significantly decreased by Sirt2 inhibitors [6]. The effect of Sirt2 on cell proliferation seems to vary in a tissue-specific and disease-specific manner; thus, the role of Sirt2 in myoblast proliferation is to be elucidated. The present study aimed to elucidate the effect of Sirt2 on C2C12 cell proliferation and cell cycle progression by infecting C2C12 cells with a recombinant adenovirus encoding Sirt2 gene.