Extracellular vesicles derived from pediatric nonalcoholic fatty liver disease (NAFLD) patient plasma induce fibrotic activation in human hepatic stellate cell culture
Extracellular vesicle (EV) communication is one of the factors that advances the development of non-alcoholic fatty liver disease (NAFLD). The expression of the genes Collagen 1 (COL1A1) and smooth muscle actin (ACTA2) is increased when the hepatic stellate cells of the liver are activated contributing to fibrosis and fatty liver. Understanding the differences in gene expression and the factors that contribute to fatty liver is the first step to creating specialized treatment plans for NAFLD. To better understand this pathway, EVs were isolated from a TGen volunteer, an obese patient, and obese patients who also had NAFLD plasma and applied to human hematopoietic stem cells (HSC) in culture. After 24 hours of EV treatment, the HSCs were harvested and the RNA was extracted to make cDNA for qPCR. The expression of COL1A1 did not increase in comparison between the EV treatment groups and control. However, the expression of ACTA2 was significantly reduced in comparison between the control and EV treatment groups. These results indicate that a better way of isolating NAFLD specific EVs might be necessary to induce the increased expression in culture.