Author of

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  P1.04 - Poster Session/ Biology, Pathology, and Molecular Testing (ID 233)

  • Event: WCLC 2015
  • Type: Poster
  • Track: Biology, Pathology, and Molecular Testing
  • Presentations: 1
  • Moderators:
  • Coordinates: 9/07/2015, 09:30 - 17:00, Exhibit Hall (Hall B+C)

  • 13659

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    P1.04-079 - RBM5-Wnt/β-Catenin Signaling in Cigarette Smoke PM 2.5 Induced Alveolar Epithelial Injury and Its Molecular Mechanism (ID 1104)

    09:30 - 09:30  |  Author(s): L.X. Jiao
    • Abstract
    • Slides

    Background:
    Tobacco related death has become the first cause of death worldwide and it is estimated that approximately 1 millions patients each year died from tobacco related diseases in China ,the most common diseases from which are COPD and lung cancer.Recently,the effects of long-term exposure to PM2.5(particulate matter) on human health have drawn much attention from clinicians and researches.Cigarette smoke is one of the main sources of indoor PM2.5. At the same time, cigarette smoke also includes nearly six thousand kinds of chemical substances, most of which are harmful to the body, especially benzopyrene.It is proved that benzopyrene is a class of organic compounds with significant carcinogenic effect. However, the underlying mechanisms remain unclear. The aims of this study were to determine the involvement of RNA-binding motif protein 5 (RBM5) and Wnt/β-catenin signaling in cigarette smoke PM2.5 induced alveolar epithelial injury, as well as the interaction between both.
    
    Methods:
    A549 cells were treated with cigarette smoke extract (CSE). The MTT assay was used to assess the effects of CSE on cell viability. The levels of RBM5 and Wnt/β-catenin/GSK3β were detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and western blots. A luciferase assay was used to assess the activity of β-catenin/TCF signaling
    
    Results:
    CSE inhibits the proliferation of A549 cells, with increasing CSE concentration and action time, the growth inhibition rate of A549 cells is more big, has the time and dose dependence; Cytosolic and nuclear β-catenin levels significantly increased following CSE treatment, compared with those in control cells (P < 0.05); The luciferase activity in CSE-exposed cells transfected with the TCF luciferase reporter wild-type plasmid (pGL3-OT) was significantly greater than that in cells without CSE exposure (33,167 ± 3085 vs. 19,978 ± 1916, respectively, P < 0.05);given CSE A549 cells, RBM5 mRNA increased with the increase of CSE concentration and action time prolonged expression gradually decreased, with time and dose dependence; with increasing concentrations of cigarette smoke extract, reduce the expression of RBM5 protein expression, with dose dependent(all P < 0.05);after pcDNA3.1-RBM5 transfection, Wnt/β-catenin signaling pathway inhibition; siRBM5 after transfection, Wnt/β-catenin signaling enhanced; give the Wnt signal pathway blocker ICG-001 blocked Wnt/β-catenin signaling pathway, the expression of RBM5 and the difference was not statistically significant.
    
    Conclusion:
    Down regulation of RBM5 and activation of Wnt/β-catenin signaling are involved in CSE PM 2.5 induced alveolar epithelial injury. RBM5 acts as an upstream molecule that negatively regulates the activity of Wnt/β-catenin signaling This study was supported by grants from the National Natural Science Foundation of China (No.81472169 and No.81241069)
    
    

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