Photo Credit: Mohammed Haneefa Nizamudeen
The following is a summary of “lnc-HC ameliorates steatosis by promoting miR-130b-3p biogenesis and the assembly of an RNA-induced silencing complex,” published in the December 2023 issue of Endocrinology by Lan, et al.
Non-alcoholic fatty liver disease (NAFLD) is mostly caused by lipid buildup in the liver. In the earlier work, researchers found that lnc-HC stops NAFLD by raising the level of miR-130b-3p. For a study, researchers found that lnc-HC, a lncRNA generated from hepatocytes, positively controls miR-130b-3p development at various levels and helps it do its job by making it easier for an RNA-induced silencing complex (RISC) to form. lnc-HC lowers the levels of genes that are affected by miR-130b-3p.
These genes include PPARγ, Acsl1, and Acsl4, which stop the buildup of fat droplets in the liver. Specifically, lnc-HC increased the promoter activity of miR-130b-3p by increasing the levels of the transcription factors Mafb and Jun. Then, lnc-HC helped with the processing step of primary miR-130b and made the connection between the Drosha enzyme and the 5′-flanking sequence of pri-miR-130b stronger so that more precursor transcripts could be made. Through direct contact with the chaperone heat shock protein 90 alpha family class A member 1 (HSP90AA1), lnc-HC helped put together RISC, which was made up of HSP90AA1, AGO2, and miR-130b-3p.
They confirmed that the expression of lnc-HC/miR-130b-3p in the liver was negatively correlated with that of the target genes and was closely linked to the concentration of triglycerides in the liver in a model that was caused by high-fat and high-cholesterol diets. These results helped them learn more about how lnc-HC controls the breakdown of fats in the liver and the development of NAFLD.
Source: sciencedirect.com/science/article/abs/pii/S0303720723002125
