• Yuhang Lin, Zhitao Zeng, and Kechuan Pan.
• Department of Infection, The First People's Hospital of Wenling, Wenling, China.
• Shock. 2023 May 1; 59 (5): 734743734-743.

AbstractPurpose: This study is designed to explore the role and mechanism of circ_0099188 in LPS-engendered HPAEpiC cells. Methods: Circ_0099188, microRNA-1236-3p (miR-1236-3p), and high mobility group box 3 (HMGB3) levels were measured using real-time quantitative polymerase chain reaction. Cell viability and apoptosis were assessed using cell counting kit-8 (CCK-8) and flow cytometry assays. Protein levels of B-cell lymphoma-2 (Bcl-2), Bcl-2 related X protein (Bax), cleaved-caspase 3, cleaved-caspase 9, and HMGB3 were determined using Western blot assay. IL-6, IL-8, IL-1β, and TNF-α levels were analyzed using enzyme-linked immunosorbent assays. After predicting using Circinteractome and Targetscan, the binding between miR-1236-3p and circ_0099188 or HMGB3 was verified using a dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays. Results: Circ_0099188 and HMGB3 were highly expressed, and miR-1236-3p was decreased in LPS-stimulated HPAEpiC cells. Also, the downregulation of circ_0099188 might overturn LPS-triggered HPAEpiC cell proliferation, apoptosis, and inflammatory response. Mechanically, circ_0099188 is able to affect HMGB3 expression by sponging miR-1236-3p. Conclusion: Circ_0099188 knockdown might mitigate LPS-induced HPAEpiC cell injury by targeting the miR-1236-3p/HMGB3 axis, providing an underlying therapeutic strategy for pneumonia treatment.Copyright © 2023 by the Shock Society.

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