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Article Open Access

LCMR1 deficiency exacerbates LPS‑induced lung injury in lung‑on‑a‑chip and mouse models

  • Authors:
    • Zhenfei Mo
    • Chengcheng Su
    • Jinxia Liu
    • Jiabo Ren
    • Lu Liu
    • Yueming Wang
    • Yanqin Li
    • Chunsun Li
    • Zhen Yang
    • Xiuqing Ma
    • Liangan Chen
  • View Affiliations / Copyright

    Affiliations: Medical School of Chinese People's Liberation Army, Chinese People's Liberation Army General Hospital, Beijing 100853, P.R. China, Department of Nutrition, The First Medical Centre, Chinese People's Liberation Army General Hospital, Beijing 100853, P.R. China, Department of Pulmonary and Critical Care Medicine, The Eighth Medical Centre, Chinese People's Liberation Army General Hospital, Beijing 100853, P.R. China, Department of Pulmonary and Critical Care Medicine, The First Medical Centre, Chinese People's Liberation Army General Hospital, Beijing 100853, P.R. China
    Copyright: © Mo et al. This is an open access article distributed under the terms of Creative Commons Attribution License.
  • Article Number: 189
    |
    Published online on: May 2, 2025
       https://doi.org/10.3892/mmr.2025.13554
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Abstract

The oncogene lung cancer metastasis‑related protein 1 (LCMR1) is associated with neoplastic diseases and LCMR1 conditional knockout affects cell homeostasis. In the present study, the role of LCMR1 in lipopolysaccharide (LPS)‑induced acute lung injury (ALI) was investigated. Firstly, wild‑type C57BL/6 mice were used to establish an LPS‑induced ALI model via intratracheal injection of LPS, and the expression of LCMR1 was examined at 24, 48, 72 and 96 h after injury. The LPS‑induced lung injury model was subsequently constructed in mice with conditional knockout of LCMR1 in type II alveolar epithelial cells (AEC‑II). Subsequently, histopathological analysis, lung wet/dry weight ratio comparisons and lung function tests were performed; survival rates after LPS challenge of the conditional knockout mice were measured; bronchoalveolar lavage fluid (BALF) was collected, and the concentrations of protein and inflammatory cytokines in BALF were measured; and transmission electron microscopy of lung tissue was conducted to evaluate the degree of lung injury. To further investigate the mechanism, a lung‑on‑a‑chip model with overexpression or knockdown of LCMR1 was constructed to simulate the alveolar environment under LPS treatment. The expression levels of E‑cadherin and pro‑pulmonary surfactant C precursor (proSP‑C) in the chips were determined by immunofluorescence, and the integrity of the air‑blood barrier was analyzed using a permeability assay. In the mouse model, LCMR1 expression was downregulated in wild‑type mice with LPS‑induced lung injury. LCMR1 conditional knockout in AEC‑II caused increased mortality, impaired lung function, aggravated pathological damage and increased the inflammatory response in mice with LPS‑induced ALI. Furthermore, in the lung‑on‑a‑chip model, LCMR1 knockdown reduced the expression of E‑cadherin and proSP‑C, and impaired the air‑blood barrier function, whereas LCMR1 overexpression attenuated these effects, which may be related to cell differentiation dysfunction and enhanced apoptosis. In conclusion, the present study revealed that LCMR1 deficiency may exacerbate LPS‑induced ALI and could be considered a novel target for intervention in ALI.
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Copy and paste a formatted citation
Spandidos Publications style
Mo Z, Su C, Liu J, Ren J, Liu L, Wang Y, Li Y, Li C, Yang Z, Ma X, Ma X, et al: <em>LCMR1</em> deficiency exacerbates LPS‑induced lung injury in lung‑on‑a‑chip and mouse models. Mol Med Rep 32: 189, 2025.
APA
Mo, Z., Su, C., Liu, J., Ren, J., Liu, L., Wang, Y. ... Chen, L. (2025). <em>LCMR1</em> deficiency exacerbates LPS‑induced lung injury in lung‑on‑a‑chip and mouse models. Molecular Medicine Reports, 32, 189. https://doi.org/10.3892/mmr.2025.13554
MLA
Mo, Z., Su, C., Liu, J., Ren, J., Liu, L., Wang, Y., Li, Y., Li, C., Yang, Z., Ma, X., Chen, L."<em>LCMR1</em> deficiency exacerbates LPS‑induced lung injury in lung‑on‑a‑chip and mouse models". Molecular Medicine Reports 32.1 (2025): 189.
Chicago
Mo, Z., Su, C., Liu, J., Ren, J., Liu, L., Wang, Y., Li, Y., Li, C., Yang, Z., Ma, X., Chen, L."<em>LCMR1</em> deficiency exacerbates LPS‑induced lung injury in lung‑on‑a‑chip and mouse models". Molecular Medicine Reports 32, no. 1 (2025): 189. https://doi.org/10.3892/mmr.2025.13554
Copy and paste a formatted citation
x
Spandidos Publications style
Mo Z, Su C, Liu J, Ren J, Liu L, Wang Y, Li Y, Li C, Yang Z, Ma X, Ma X, et al: <em>LCMR1</em> deficiency exacerbates LPS‑induced lung injury in lung‑on‑a‑chip and mouse models. Mol Med Rep 32: 189, 2025.
APA
Mo, Z., Su, C., Liu, J., Ren, J., Liu, L., Wang, Y. ... Chen, L. (2025). <em>LCMR1</em> deficiency exacerbates LPS‑induced lung injury in lung‑on‑a‑chip and mouse models. Molecular Medicine Reports, 32, 189. https://doi.org/10.3892/mmr.2025.13554
MLA
Mo, Z., Su, C., Liu, J., Ren, J., Liu, L., Wang, Y., Li, Y., Li, C., Yang, Z., Ma, X., Chen, L."<em>LCMR1</em> deficiency exacerbates LPS‑induced lung injury in lung‑on‑a‑chip and mouse models". Molecular Medicine Reports 32.1 (2025): 189.
Chicago
Mo, Z., Su, C., Liu, J., Ren, J., Liu, L., Wang, Y., Li, Y., Li, C., Yang, Z., Ma, X., Chen, L."<em>LCMR1</em> deficiency exacerbates LPS‑induced lung injury in lung‑on‑a‑chip and mouse models". Molecular Medicine Reports 32, no. 1 (2025): 189. https://doi.org/10.3892/mmr.2025.13554
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