The role of the Gas6/TAM signal pathway in the LPS-induced pulmonary epithelial cells injury.

Autor: Cheng Y; Department of Blood Transfusion, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, 650032 Kunming, Yunnan, China., Yang X; Department of Blood Transfusion, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, 650032 Kunming, Yunnan, China., Wang Y; Department of Blood Transfusion, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, 650032 Kunming, Yunnan, China., Ding Q; Blood Center of Hani-Yi Autonomous Prefecture of Honghe, 661000 Mengzi, Yunnan, China., Huang Y; Blood Center of Hani-Yi Autonomous Prefecture of Honghe, 661000 Mengzi, Yunnan, China., Zhang C; Department of Blood Transfusion, The First People's Hospital of Yunnan Province, The Affiliated Hospital of Kunming University of Science and Technology, 650032 Kunming, Yunnan, China. Electronic address: zhangchanyzt@163.com.
Jazyk: angličtina
Zdroj: Molecular immunology [Mol Immunol] 2023 Nov; Vol. 163, pp. 181-187. Date of Electronic Publication: 2023 Oct 09.
DOI: 10.1016/j.molimm.2023.10.001
Abstrakt: Background: Acute lung injury (ALI) is an acute inflammatory respiratory disease. The interaction between growth arrest-specific 6 (Gas6) and tyrosine kinases of the Tyro3, Axl, Mer (TAM) family plays an important role in a variety of physiological and pathological processes, including inflammation. In this study, we mainly clarified the mechanism of the Gas6/TAM signal pathway in lipopolysaccharide (LPS)-induced pulmonary epithelial cells (BEAS-2B cells) injury.
Methods: We cultured BEAS-2B cells in vitro and established a LPS-induced BEAS-2B cells injury model. Then, the siRNA sequence (siGas6-2) was transfected into cells. The expression of Gas6/TAM was measured based on quantitative reverse transcription polymerase chain reaction (qRT-RCR) and western blot (WB). Cell proliferation and apoptosis were measured by cell counting Kit-8 (CCK-8) and flow cytometry. The expression of pro-inflammatory factors was measured by qRT-RCR and WB.
Results: Our study showed that when the 40 μg/mL LPS-induced BEAS-2B cells injury model was established, cell viability was significantly reduced, but the Gas6/TAM signal pathway was activated. When transfection with siGas6-2, low expression of Gas6 directly reduced the expression of downstream TAM receptors. Furthermore, the inhibition of the Gas6/TAM signal pathway significantly reduced the occurrence of cell apoptosis and the expression of inflammatory factors, and promoted cell proliferation.
Conclusion: Our research indicated that Gas6/TAM played an important role in cell proliferation, apoptosis, and inflammatory response in the LPS-induced BEAS-2B cells injury, and Gas6/TAM may be a new target in the treatment of ALI in the future.
Competing Interests: Declaration of Competing Interest The authors declared that they have no conflicts of interest.
(Copyright © 2023 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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