Presentation description

Metabolic Dysfunction-Associated Liver Disease (MAFLD) is a condition that affects a large portion of the population and can progress into Metabolic Dysfunction-Associated Steatohepatitis (MASH), which is an advanced form of the disease. However, despite their prevalence, there are currently no treatment options that involve medication; this is because there isn't enough research on this topic to fully understand the mechanism of the disease to create informed and targeted treatment options. Because there isn't enough research on this topic to fully understand the mechanism of the disease to create informed and targeted treatment options. Current research suggests that one of the potential developments of MAFLD (and subsequently MASH), is due to these inflammatory responses. At a cellular level, these responses are initiated by a signal that ultimately sets off the cascade, resulting in the activation of pathways that will induce apoptosis. The research question involved in this investigation was specifically aimed at studying Mitochondrial Double Stranded RNA (mtdsRNA) as the cellular signal that sets off this inflammatory response cascade. This was first evaluated performing immunohistochemistry protocols and confocal imaging to determine the amount of dsRNA both with a negative control (DMSO), and with damaged hepatocytes (acetaminophen and DMSO). Once we were able to determine and quantify the difference in dsRNA content, we were then able to move into measuring the inflammatory interferon response. This was performed by isolating the RNA from hepatocytes treated with a known interferon activator, and the damaged hepatocytes, which we then converted into cDNA and quantified through PCR. This study is aimed at gaining more insight and information into dsRNA's potential role in the activation of the signaling pathway that leads to the inflammatory response cascade involved in apoptosis.