Buffalo long non-coding RNA gene11007 promotes myoblasts proliferation.

Buffalo meat is of good quality because it is lean and tender, and could bring significant cardiovascular benefits. The underlying difference in muscle development and meat quality is a complex and precisely orchestrated process which has been demonstrated to be regulated by long non-coding RNAs (lncRNAs). However, the regulatory role of lncRNAs in the growth and development of buffalo skeletal muscle is still unclear. In this study, the Ribo-Zero RNA-Seq method was used to explore the lncRNA expression profiles of buffalo myoblasts during the proliferation and differentiation phases. A specific set of 9,978 lncRNAs was found. By comparing the expression profiles of lncRNAs, it was found that there were 1,576 differentially expressed lncRNAs (DELs) during buffalo myoblast differentiation. Twelve DELs were chosen and subsequently verified in eight different buffalo tissues during fetal and adult stages by using qPCR. Gene11007 was found to be one of the most down-regulated lncRNAs during buffalo myoblasts differentiation and it was subsequently characterized. EdU, CCK-8, qPCR and western blotting assays showed that gene11007 promoted the proliferation of buffalo myoblasts but it had no effect on cell differentiation. Our research may enrich the genome annotations of buffalo and provide a new molecular target for the in-depth understanding of the regulation of lncRNAs in skeletal muscle.

Discovery of Differentially Expressed MicroRNAs in Porcine Ovaries With Smaller and Larger Litter Size.

The number of live births in a litter is an important reproductive trait, and is one of the main indicators which reflect the production level and economic benefit of a pig farm. The ovary is an important reproductive organ of the sow, and it undergoes a series of biological processes during each estrous cycle. A complex transcriptional network containing coding and non-coding RNAs in the ovary closely regulates the reproductive capability of sows. However, the molecular regulation mechanisms affecting sow litter size are still unclear. We investigated the expression profiles of microRNAs (miRNAs) in porcine ovaries from sows with smaller than average litter sizes (SLS) and those with larger litter sizes (LLS). In total, 411 miRNAs were identified, and of these 17 were significantly down-regulated and 16 miRNAs were up-regulated when comparing sows with LLS and SLS, respectively. We further characterized the role of miR-183 which was one of the most up-regulated miRNAs. CCK-8, EdU incorporation and western blotting assays demonstrated that miR-183 promoted the proliferation of granulosa cells (GCs) in pig ovaries. Moreover, miR-183 inhibited the synthesis of estradiol in GCs and promoted the synthesis of progesterone. These results will help in gaining understanding of the role of miRNAs in regulating porcine litter size.

GosB Inhibits Triacylglycerol Synthesis and Promotes Cell Survival in Mouse Mammary Epithelial Cells.

It has been demonstrated that the activator protein related transcription factor Finkel-Biskis-Jinkins murine osteosarcoma B (GosB) is involved in preadipocyte differentiation and triacylglycerol synthesis. However, the role of GosB in regulating the synthesis of milk fatty acid in mouse mammary glands remains unclear. This research uncovered potentially new roles of GosB in suppressing milk fatty acid synthesis. Results revealed that GosB had the highest expression in lung tissue and showed a higher expression level during nonlactation than during lactation. GosB inhibited the expression of fatty acid synthase (FASN), stearoyl-CoA desaturase (SCD), fatty acid binding protein 4 (FABP4), diacylglycerol acyltransferase 1 (DGAT1), perilipin 2 (PLIN2), perilipin 3 (PLIN3), and C/EBPα in mouse mammary gland epithelial cells (MEC). In addition, GosB reduced cellular triglyceride content and the accumulation of lipid droplets; in particular, GosB enhanced saturated fatty acid concentration (C16:0 and C18:0). The PPARγ agonist, rosiglitazone (ROSI), promoted apoptosis and inhibited cell proliferation. GosB increased the expression of Bcl-2 and protected MEC from ROSI-induced apoptosis. Furthermore, MECs were protected from apoptosis through the GosB regulation of intracellular calcium concentrations. These findings suggest that GosB may regulate mammary epithelial cells milk fat synthesis and apoptosis via PPARγ in mouse mammary glands.