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    Activated platelets rescue apoptotic cells via paracrine activation of EGFR and DNA-dependent protein kinase.

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    Author
    Au, AE-L; Sashindranath, M; Borg, RJ; Kleifeld, O; Andrews, RK; Gardiner, EE; Medcalf, RL; Samson, AL
    Date
    2014-09-11
    Source Title
    Cell Death and Disease
    Publisher
    Springer Science and Business Media LLC
    University of Melbourne Author/s
    Au, Amanda
    Affiliation
    Medical Biology (W.E.H.I.)
    Metadata
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    Document Type
    Journal Article
    Citations
    Au, A. E. -L., Sashindranath, M., Borg, R. J., Kleifeld, O., Andrews, R. K., Gardiner, E. E., Medcalf, R. L. & Samson, A. L. (2014). Activated platelets rescue apoptotic cells via paracrine activation of EGFR and DNA-dependent protein kinase.. Cell Death Dis, 5 (9), pp.e1410-. https://doi.org/10.1038/cddis.2014.373.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/256222
    DOI
    10.1038/cddis.2014.373
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4540201
    Abstract
    Platelet activation is a frontline response to injury, not only essential for clot formation but also important for tissue repair. Indeed, the reparative influence of platelets has long been exploited therapeutically where application of platelet concentrates expedites wound recovery. Despite this, the mechanisms of platelet-triggered cytoprotection are poorly understood. Here, we show that activated platelets accumulate in the brain to exceptionally high levels following injury and release factors that potently protect neurons from apoptosis. Kinomic microarray and subsequent kinase inhibitor studies showed that platelet-based neuroprotection relies upon paracrine activation of the epidermal growth factor receptor (EGFR) and downstream DNA-dependent protein kinase (DNA-PK). This same anti-apoptotic cascade stimulated by activated platelets also provided chemo-resistance to several cancer cell types. Surprisingly, deep proteomic profiling of the platelet releasate failed to identify any known EGFR ligand, indicating that activated platelets release an atypical activator of the EGFR. This study is the first to formally associate platelet activation to EGFR/DNA-PK--an endogenous cytoprotective cascade.

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