RhoA regulates lipopolysaccharide‑induced lung cell injury via the Wnt/β‑catenin pathway

  • Authors:
    • Guanhua Chen
    • Xuedong Sun
    • Chunxiao Dong
  • View Affiliations

  • Published online on: September 29, 2017     https://doi.org/10.3892/mmr.2017.7662
  • Pages:8501-8506
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Abstract

Ras homolog family member A (RhoA) has been reported to be involved in numerous biological processes; however, the effects of RhoA on acute lung injury (ALI) have yet to be reported. The present study aimed to explore how RhoA affects cell viability, reactive oxygen species (ROS) activity and cell apoptosis in a cell model of lipopolysaccharide (LPS)‑induced ALI. An MTT assay, flow cytometry, reverse transcription‑quantitative polymerase chain reaction and western blotting were used to determine the effects of RhoA on cell viability, apoptosis and ROS activity. The results demonstrated that RhoA inactivation was able to promote cell viability, and decrease apoptosis and ROS activity of LPS‑treated cells. The results of western blotting indicated that RhoA activated the downstream Wnt/β‑catenin signaling pathway and inhibited the expression of apoptotic factors. These findings suggested that RhoA may be involved in ALI progression and could be a novel therapeutic target for this disease.

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December 2017
Volume 16 Issue 6

Print ISSN: 1791-2997
Online ISSN:1791-3004

2016 Impact Factor: 1.692
Ranked #19/128 Medicine Research and Experimental
(total number of cites)

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APA
Chen, G., Sun, X., & Dong, C. (2017). RhoA regulates lipopolysaccharide‑induced lung cell injury via the Wnt/β‑catenin pathway. Molecular Medicine Reports, 16, 8501-8506. https://doi.org/10.3892/mmr.2017.7662
MLA
Chen, G., Sun, X., Dong, C."RhoA regulates lipopolysaccharide‑induced lung cell injury via the Wnt/β‑catenin pathway". Molecular Medicine Reports 16.6 (2017): 8501-8506.
Chicago
Chen, G., Sun, X., Dong, C."RhoA regulates lipopolysaccharide‑induced lung cell injury via the Wnt/β‑catenin pathway". Molecular Medicine Reports 16, no. 6 (2017): 8501-8506. https://doi.org/10.3892/mmr.2017.7662