Home General Physiology and Biophysics 2025 General Physiology and Biophysics Vol.44, No.5, p. 391–403, 2025

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ISSN 1338-4325 (online)
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General Physiology and Biophysics Vol.44, No.5, p. 391–403, 2025

Title: circ_0049271 downregulation ameliorates lipopolysaccharide-induced human renal tubular endothelial cell apoptosis, inflammation and oxidative stress
Author: Xiaozhen Ji, Jinjuan Zhang, Lefeng Zhang
Abstract: Circular RNA (circRNA) has been confirmed to be a regulator for septic acute kidney injury (AKI). It is reported that circ_0049271 has abnormal expression in AKI patients, but its role and mechanism in septic AKI remain unclear. Lipopolysaccharide (LPS)-stimulated HK-2 cells were served as the cellular model of sepsis-associated AKI (SAKI). qRT-PCR was conducted for examining the expression of circ_0049271, KEAP1 and miR-331-3p. Cell proliferation and apoptosis were detected by EdU assay and flow cytometry. The protein levels of apoptosis-related markers, RUNX family transcription factor 1 (RUNX1), and PI3K/AKT/mTOR pathway-related markers were tested using Western blot. RNA interaction was confirmed by dual-luciferase reporter assay, RIP assay, and RNA pull-down assay. Our data showed that circ_0049271 was enhanced in LPS-induced HK-2 cells. Silencing of circ_0049271 attenuated LPS-induced HK-2 cell oxidative stress, apoptosis, and inflammation. In terms of mechanism, circ_0049271 targeted miR-331-3p to promote LPS-induced HK-2 cell injury. RUNX1 was a target of miR-331-3p, and RUNX1 overexpression reversed miR-331-3p-mediated inhibitory effects on LPS-induced HK-2 cell injury. Moreover, circ_0049271 sponged miR-331-3p to positively regulate RUNX1 expression, thus activating the PI3K/AKT/mTOR pathway. In conclusion, our data indicated that circ_0049271 contributed to LPS-induced HK-2 cell injury by regulating miR-331-3p/RUNX1 pathway, providing potential molecular targets for the treatment of SAKI.
Keywords: Sepsis — SAKI — circ_0049271 — miR-331-3p — RUNX1
Year: 2025, Volume: 44, Issue: 5 Page From: 391, Page To: 403
doi:10.4149/gpb_2025024


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