ABSTRACT
OBJECTIVE: High mobility group AT-hook 2 (HMGA2) has been increasingly acknowledged to be significantly expressed in malignant tumors. However, it has been discovered to serve as a pro-inflammatory factor in several diseases. This study aimed to investigate the involvement of HMGA2 in septic lung injury. METHODS: Human pulmonary alveolar epithelial cells were subjected to lipopolysaccharide (LPS) to construct models. The effects of HMGA2 knockdown on cell viability, inflammation, and apoptosis were evaluated. Following the verification of the association between HMGA2 and Enhancer of Zeste homolog 2 (EZH2), the impacts of EZH2 on HMGA2 regulation were determined. RESULTS: The levels of HMGA2 in the LPS-treated cells were all significantly elevated. HMGA2 knockdown alleviated damage caused by LPS in cellular viability, and reduced inflammation and apoptosis. Whereas EZH2 overexpression reversed the impacts of HMGA2 knockdown on these aspects, indicating EZH2 participated in the regulation of HMGA2 on cells. CONCLUSION: HMGA2 could synergize with EZH2 to induce lung epithelial cell destruction in septic lung injury. Herein, targets for treatment have been investigated, which involves suppressing pro-inflammatory factors to reduce the body's inflammatory response.
