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Updated: Jan 12, 2026
Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
SENP5 Attenuates LPS-Induced Acute Lung Injury by Inhibiting Apoptosis of Lung Epithelial Cells Through SLC7A5/mTOR
Yiran He1, Hai Zhang2, Jianmin Gu3
1Department of Critical Care Medicine, Zhongshan Hospital, Fudan University, 200032 Shanghai, China.
Objective:
Small ubiquitin-related modifier protein (SUMO)ylation is a reversible post-translational modification of proteins. SENP5, a SUMO-specific protease, plays key roles in a wide range of cellular processes. This study aims to investigate the potential involvement of SENP5 in lipopolysaccharide (LPS)-induced acute lung injury (ALI).
Methods:
First, we established LPS-treated human normal lung epithelial cells (BEAS-2B) and a lung injury mouse model. SENP5 expression was then analyzed in vivo and in vitro using quantitative real-time PCR (qRT-PCR), Western blot, hematoxylin-eosin (H&E) staining, and immunohistochemistry. Then, CCK-8 assay and flow cytometry were employed to assess inflammatory response and apoptosis following SENP5 knockdown in LPS-induced BEAS-2B cells. Next, H&E, immunohistochemistry, and survival analysis were conducted to investigate apoptosis and proliferation in SENP5 conditional knockout (cKO) mice. Finally, RNA sequencing was used to screen for differentially expressed genes in SENP5 knockdown BEAS-2B cells. Downstream molecules and signaling pathways were analyzed using Western blot and qRT-PCR.
Results:
SENP5 was notably upregulated in both LPS-induced BEAS-2B cells and the lung injury mouse model. In vitro, SENP5 knockdown markedly exacerbated the LPS-induced suppression of BEAS-2B cell viability and promoted inflammatory response and apoptosis. Besides, the conditional knockout of SENP5 significantly increased apoptosis and inhibited proliferation in the lungs of mice. RNA sequencing indicated SENP5 deficiency inhibited solute carrier family 7 member 5/mechanistic target of rapamycin (SLC7A5/mTOR) signaling in LPS-induced BEAS-2B cells. Therefore, we confirmed that SENP5 might exert a protective effect against LPS-induced lung injury by inhibiting apoptosis of lung epithelial cells through the SLC7A5/mTOR signaling pathway.
Conclusion:
SENP5 might play a protective role in LPS-induced lung injury by inhibiting apoptosis of lung epithelial cells through the SLC7A5/mTOR signaling pathway.
