Curtin University Homepage
  • Library
  • Help
    • Admin

    espace - Curtin’s institutional repository

    JavaScript is disabled for your browser. Some features of this site may not work without it.
    View Item 
    • espace Home
    • espace
    • Curtin Research Publications
    • View Item
    • espace Home
    • espace
    • Curtin Research Publications
    • View Item

    Heat shock factor 4 regulates lens epithelial cell homeostasis by working with lysosome and anti-apoptosis pathways

    Access Status
    Fulltext not available
    Authors
    Cui, X.
    Liu, H.
    Li, J.
    Guo, K.
    Han, W.
    Dong, Y.
    Wan, S.
    Wang, Xuan-Ce
    Jia, P.
    Li, S.
    Ma, Y.
    Zhang, J.
    Mu, H.
    Hu, Y.
    Date
    2016
    Type
    Journal Article
    
    Metadata
    Show full item record
    Citation
    Cui, X. and Liu, H. and Li, J. and Guo, K. and Han, W. and Dong, Y. and Wan, S. et al. 2016. Heat shock factor 4 regulates lens epithelial cell homeostasis by working with lysosome and anti-apoptosis pathways. International Journal of Biochemistry and Cell Biology. 79: pp. 118-127.
    Source Title
    International Journal of Biochemistry and Cell Biology
    DOI
    10.1016/j.biocel.2016.08.022
    ISSN
    1357-2725
    School
    School of Earth and Planetary Sciences (EPS)
    URI
    http://hdl.handle.net/20.500.11937/65429
    Collection
    • Curtin Research Publications
    Abstract

    © 2016 Elsevier Ltd Activation of Heat shock factor 4-mediated heat shock response is closely associated with postnatal lens development. HSF4 controls the expression of small heat shock proteins (e.g. HSP25 and CRYAB) in lens epithelial cells. However, their roles in modulating lens epithelium homeostasis remain unclear. In this paper, we find that HSF4 is developmentally expressed in mouse lens epithelium and fiber tissue. HSF4 and alpha B-crystallin can selectively protect lens epithelial cells from cisplatin and H2O2 induced apoptosis by stabilizing mitochondrial membrane potential (?Y m ) and reducing ROS production. In addition, to our surprise, HSF4 is involved in upregulating lysosome activity. We found mLEC/HA-Hsf4 cells to have increased DLAD expression, lysosome acidity, cathepsin B activity, and degradation of plasmid DNA and GFP-LC3 protein when compared to mLEC/Hsf4-/- cells. Knocking down Cryab from mLEC/HA-Hsf4 cells inhibits HSF4-mediated lysosome acidification, while overexpression of CRYAB can upregulate cathepsin B activity in mLEC/Hsf4-/- cells. CRAYAB can interact with ATP6V1/A the A subunit of the H + pump vacuolar ATPase, and is colocalized to lamp1 and lamp2 in the lysosome. Collectively, these results suggest that in addition to modulating anti-apoptosis, HSF4 is able to regulate lysosome activity by at least controlling alpha B-crystallin expression, shedding light on a novel molecular mechanism of HSF4 in regulating lens epithelial cell homeostasis.

    Related items

    Showing items related by title, author, creator and subject.

    • Lysosomal cystine accumulation promotes mitochondrial depolarization and induction of redox-sensitive genes in human kidney proximal tubular cells
      Sumayao, R.; McEvoy, B.; Newsholme, Philip; McMorrow, T. (2016)
      Key points: Cystine is a disulphide amino acid that is normally generated in the lysosomes by the breakdown of cystine-containing proteins. Previously, we demonstrated that lysosomal cystine accumulation in kidney proximal ...
    • The fat cell senescence hypothesis: a mechanism responsible for abrogating the resolution of inflammation in chronic disease
      Newsholme, Philip; de Bittencourt, P. (2014)
      Purpose of review: Obesity is a chronic inflammatory disease in which the physiological resolution of inflammation is attenuated, leading to low-grade inflammation throughout the body. However, the heat shock response, ...
    • Dysregulated repair in asthmatic paediatric airway epithelial cells: The role of plasminogen activator inhibitor-1
      Stevens, P.T.; Kicic, Anthony ; Sutanto, E.N.; Knight, D.A.; Stick, S.M. (2008)
      Background: Asthma is associated with structural changes to airways such as extracellular matrix deposition and epithelial damage. Evidence suggests that asthmatic airway epithelial repair is abnormal and that elevated ...
    Advanced search

    Browse

    Communities & CollectionsIssue DateAuthorTitleSubjectDocument TypeThis CollectionIssue DateAuthorTitleSubjectDocument Type

    My Account

    Admin

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular Authors

    Follow Curtin

    • 
    • 
    • 
    • 
    • 

    CRICOS Provider Code: 00301JABN: 99 143 842 569TEQSA: PRV12158

    Copyright | Disclaimer | Privacy statement | Accessibility

    Curtin would like to pay respect to the Aboriginal and Torres Strait Islander members of our community by acknowledging the traditional owners of the land on which the Perth campus is located, the Whadjuk people of the Nyungar Nation; and on our Kalgoorlie campus, the Wongutha people of the North-Eastern Goldfields.