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  • Title: Neuroprotective effect of FMS-like tyrosine kinase-3 silence on cerebral ischemia/reperfusion injury in a SH-SY5Y cell line.
    Author: Dong RF, Tai LW, Zhang B, Shi FK, Liu HM, Duan PC, Cheng Y.
    Journal: Gene; 2019 May 20; 697():152-158. PubMed ID: 30772520.
    Abstract:
    Neuron damage contributes to ischemic brain injury. Although FMS-like tyrosine kinase-3 (FLT3) plays a critical role in neuron survival, its function and molecular mechanism in cerebral ischemia/reperfusion injury is unclear. In the present study, we exposed SH-SY5Y cells to oxygen and glucose deprivation/reoxygenation (OGD/R) to mimic ischemia/reperfusion injury. We found that FLT3 and MAPK14/p38α expression increased in OGD/R-treated cells. FLT3 silence significantly increased OGD/R-induced SH-SY5Y cell survival, inhibited reactive oxygen species production. Also, we observed that FLT3 silence suppressed OGD/R-induced SH-SY5Y cell apoptosis, apoptosis related protein Bax level and caspase-3 activity was decreased and Bcl-2 expression was increased in FLT3 silence SH-SY5Y cell treated with OGD/R. Furthermore, FLT3 depletion induced MAPK14/p38α inhibition in SH-SY5Y cultures after OGD/R exposure. These findings suggest that MAPK14/p38α overexpression reverses the action of FLT3 silence in OGD/R-induced SH-SY5Y cells. They also provide the first evidence that FLT3 silence has a neuroprotective role in OGD/R-induced SH-SY5Y cell damage. These data provide insight about potential neuroprotective molecular for ischemia/reperfusion injury.
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