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

  • Mol Immunol. 2023 Oct 9:163:181-187. doi: 10.1016/j.molimm.2023.10.001.
Yujing Cheng  1 ,  Xin Yang  1 ,  Ying Wang  1 ,  Quan Ding  2 ,  Yu Huang  2 ,  Chan Zhang  3
Affiliations
  • 1. 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.
  • 2. Blood Center of Hani-Yi Autonomous Prefecture of Honghe, 661000 Mengzi, Yunnan, China.
  • 3. 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: [email protected].
PMID: 37820442 DOI: 10.1016/j.molimm.2023.10.001
Abstract

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.

Keywords
Acute lung injury; Apoptosis; Gas6/TAM signal pathway; Inflammation; Proliferation.
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