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    Biphasic effects of autophagy on decompression bubble-induced endothelial injury

    79719.pdf (1.263Mb)
    Access Status
    Open access
    Authors
    Wang, M.
    Zhang, K.
    Nie, S.
    Huang, G.
    Yi, H.
    He, C.
    Buzzacott, Peter
    Xu, W.
    Date
    2019
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Wang, M. and Zhang, K. and Nie, S. and Huang, G. and Yi, H. and He, C. and Buzzacott, P. et al. 2019. Biphasic effects of autophagy on decompression bubble-induced endothelial injury. Journal of Cellular and Molecular Medicine. 23 (12): pp. 8058-8066.
    Source Title
    Journal of Cellular and Molecular Medicine
    DOI
    10.1111/jcmm.14672
    Additional URLs
    http://creativecommons.org/licenses/by/4.0/
    ISSN
    1582-1838
    Faculty
    Faculty of Health Sciences
    School
    School of Nursing, Midwifery and Paramedicine
    URI
    http://hdl.handle.net/20.500.11937/79637
    Collection
    • Curtin Research Publications
    Abstract

    Endothelial dysfunction induced by bubbles plays an important role in decompression sickness (DCS), but the mechanism of which has not been clear. The present study was to investigate the role of autophagy in bubble-induced endothelial injury. Human umbilical vein endothelial cells (HUVECs) were treated with bubbles, autophagy markers and endothelial injury indices were determined, and relationship strengths were quantified. Effects of autophagy inhibitor 3-methyladenine (3-MA) were observed. Bubble contact for 1, 5, 10, 20 or 30 minutes induced significant autophagy with increases in LC3-II/I ratio and Beclin-1, and a decrease in P62, which correlated with bubble contact duration. Apoptosis rate, cytochrome C and cleaved caspase-3 increased, and cell viability decreased following bubble contact for 10, 20 or 30 minutes, but not for 1 or 5 minutes. Injuries in HUVECs were correlated with LC3-II/I ratio and partially reversed by 3-MA in 10, 20 or 30 minutes contact, but worsened in 1 or 5 minutes. Bubble pre-conditioning for 1 minutes resulted in increased cell viability and decreased apoptosis rate compared with no pre-conditioning, and 30-minutes pre-conditioning induced opposing changes, all of which were inhibited by 3-MA. In conclusion, autophagy was involved and played a biphasic role in bubble-induced endothelial injury.

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