Administration of miRNA to fatty liver model using AteloGene

Article information
Signal transducer and activator of transcription 5 plays a crucial role in hepatic lipid metabolism through regulation of CD36 expression.
Hosui A, Tatsumi T, Hikita H, Saito Y, Hiramatsu N, Tsujii M, Hennighausen L, Takehara T.
Hepatol Res. 2017 Jul;47(8):813-825. PMID: 27593674

Overview
Non-alcoholic fatty liver disease is the most common chronic liver disease in developed countries, but the pathogenic mechanism of this condition has not yet been elucidated.

The authors previously reported that liver-specific STAT5-deficient mice exhibit fatty liver disease. On the other hand, it is thought that glycoprotein CD36 recognizes fatty acid, LDL, and oxidized LDL, and that CD36 is involved in the migration of adipocytes and macrophages.

Therefore, the authors investigated the expression level of CD36 in the liver of the STAT5-deficient mouse, demonstrating that CD36 expression is markedly increased compared to a control group of disease-free mice. Expression analysis of relevant miRNAs also showed that the expression of miR-20b was decreased over two-fold compared to the control group.

The authors followed these in vitro experiments with in vivo experiments for functional evaluation of miR-20b. Notably, tail vein administration of miR-20b using AteloGene reduced the expression level of CD36 and decreased triglyceride levels in the liver of STAT5-deficient mice. These experiments demonstrated a role for miR-20b in lipid metabolism, showing that STAT5 is important for CD36 regulation.

Atelocollagen-based transfection reagent that suppresses nucleic acid degradation in vivo

Product name
– AteloGene Systemic Use（Cat. No.: #1393 for Cosmo Bio customers）
                                             (Cat. No.: #1395 for REPROCELL customers)