Background: Myostatin (Mstn), a member of the TGF-β superfamily, is a negative regulator of skeletal muscle mass in mammals. Precise regulation of Mstn expression is important for somite growth in fish. MicroRNA (miRNA), a type of small non-coding RNA, regulates gene expression at the post-transcriptional level and participates in various physiological functions. A growing amount of evidence has emphasized the importance of miRNA in the development of skeletal muscle.Aims: This study aims to study how miRNAs regulate myostatin b (mstnb) post-transcriptionally in tilapia.Methods/Results:
Mstnb 3′ UTR sequences were obtained, and the results of tissue distribution showed that mstnb was expressed in several tissues, including brain, white muscle, gut, and adipose tissue. A total of 1,992 miRNAs were predicted to target mstnb in tilapia using bioinformatics, and a dual-luciferase reporter experiment confirmed that miR-181a/b-5p, miR-30-3p, miR-200a, and miR-27a were the target miRNAs of mstnb. Mutagenesis of the miR-181b-5p binding sites of mstnb significantly increased the luciferase signal compared to the wild-type mstnb. In tilapia primary muscle cells, overexpression of miR-181b-5p led to the downregulation of MSTNb expression, and the inhibitory effect of MSTNb on the downstream genes was dismissed, while inhibition of miR-181b-5p could reverse these phenomena.Conclusion: Taken together, our results suggested that miR-181b-5p could promote the growth of skeletal muscle by decreasing the MSTNb protein level in tilapia.
Background
Non-alcoholic fatty liver disease (NAFLD) has been well defined as a common chronic liver metabolism disorder. Statins as a first-line therapeutic treatment had some side effects. Here, we found that Fumigaclavine C (FC) was collected from endophytic Aspergillus terreus via the root of Rhizophora stylosa (Rhizophoraceae), had potential anti-adipogenic and hepatoprotective effects both in vitro and in vivo without obvious adverse side effects. However, the mechanisms of the prevention and management of FC for hepatic steatosis are incompletely delineated.
Methods
The pharmacodynamic effects of FC were measured in high-fat diet (HFD)-induced obese mice. Liver index and blood biochemical were examined. Histopathological examination in the liver was performed by hematoxylin & eosin or oil red O. The levels of serum TG, TC, LDL-c, HDL-c, FFA, T-bili, ALT, AST, creatinine, and creatine kinase were estimated via diagnostic assay kits. The levels of hepatic lipid metabolism-related genes were detected via qRT-PCR. The expression levels of hepatic de novo lipogenesis were quantitated with Western blot analysis.
Results
FC-treatment markedly reduced hepatic lipid accumulation in HFD-induced obese mice. FC significantly attenuated the hepatic lipid metabolism and ameliorated liver injury without obvious adverse side effects. Moreover, FC also could dose-dependently modulate the expressions of lipid metabolism-related transcription genes. Mechanically, FC notably suppressed sterol response element binding protein-1c mediated de novo lipogenesis via interfering with the RhoA/ROCK signaling pathway by decreasing the levels of geranylgeranyl diphosphate and farnesyl diphosphate.
Conclusions
These findings suggested that FC could improve hepatic steatosis through inhibiting de novo lipogenesis via modulating the RhoA/ROCK signaling pathway.
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