miR-136 Regulates the Proliferation and Adipogenic Differentiation of Adipose-Derived Stromal Vascular Fractions by Targeting HSD17B12.

Fat deposition involves the continuous differentiation of adipocytes and lipid accumulation. Studies have shown that microRNA miR-136 and 17ß-hydroxysteroid dehydrogenase type 12 (HSD17B12) play important roles in lipid accumulation. However, the regulatory mechanism through which miR-136 targets HSD17B12 during ovine adipogenesis remains unclear. This study aimed to elucidate the role of miR-136 and HSD17B12 in adipogenesis and their relationship in ovine adipose-derived stromal vascular fractions (SVFs). The target relationship between miR-136 and HSD17B12 was predicted and confirmed using bioinformatics and a dual-luciferase reporter assay. The results showed that miR-136 promoted proliferation and inhibited adipogenic differentiation of ovine SVFs. We also found that HSD17B12 inhibited proliferation and promoted adipogenic differentiation of ovine SVFs. Collectively, our results indicate that miR-136 facilitates proliferation and attenuates adipogenic differentiation of ovine SVFs by targeting HSD17B12. These findings provide a theoretical foundation for further elucidation of the regulatory mechanisms of lipid deposition in sheep.

LncRNAs as the Regulators of Brain Function and Therapeutic Targets for Alzheimer's Disease.

Alzheimer's disease (AD) is the most common type of dementia and a serious threat to the health and safety of the elderly population. It has become an emerging public health problem and a major economic and social burden. However, there is currently no effective treatment for AD. Although the mechanism of AD pathogenesis has been investigated substantially, the full range of molecular factors that contribute to its development remain largely unclear. In recent years, accumulating evidence has revealed that long non-coding RNAs (lncRNAs), a type of non-coding RNA longer than 200 nucleotides, play important roles in multiple biological processes involved in AD pathogenesis. With the further exploration of genomics, the role of lncRNA in the pathogenesis of AD has been phenotypically or mechanistically studied. Herein, we systematically review the current knowledge about lncRNAs implicated in AD and elaborate on their main regulatory pathways, which may contribute to the discovery of novel therapeutic targets and drugs for AD.