Establishment of an Acid-Induced Het-1A Cell Model and Functional Analysis of the miR-107/FGFRL1 Axis

Extensive evidence suggests that microRNAs (miRNAs) play a key role in gastrointestinal pathophysiological processes. However, their specific mechanisms in reflux esophagitis (RE) remain poorly understood. Here, we present a protocol to establish an acid-induced RE model and to investigate the miR-107/FGFRL1 axis using molecular and cellular assays. We conducted clinical sample analyses, including serum collection from patients with R E (n=94) and healthy controls (n=94), followed by quantitative detection via RT-qPCR. In vitro, an acid-induced injury model was established using Het-1A cells exposed to hydrochloric acid. Additionally, functional validation of the cells was performed using MTT cell viability assays and dual-luciferase reporter assays. Representative results indicate that miR-107 was downregulated in the serum of RE patients and in acid-treated Het-1A cells. miR-107 mediated hydrochloric acid-induced changes in Het-1A cell viability and inflammation levels by directly targeting FGFRL1 and is associated with changes in cell viability and inflammation through FGFRL1 targeting. This protocol enables investigation of miR-107/FGFRL1-mediated mechanisms in RE. This approach provides a reproducible platform for studying molecular mechanisms in RE.