Abstract
Peptidyl prolyl isomerase (Pin1) and Death‐associated protein kinase 1 (DAPK1) have been investigated as a key factor in cell death of cerebral ischemia. But, Pin1 and DAPK1 signaling pathway have not been clearly elucidated in case of ischemia/reperfusion. Cerebral ischemia/reperfusion injury is known to be induced by imbalanced inflammation and oxidative stress. Also, recent articles identified the Ikappa B kinase (IKK), which is a main mediator of inflammation signal‐induced neuronal cell death in ischemic stroke. Here, we examined the close relationship among DAPK1, Pin1 and IKK in ischemia/reperfusion (I/R). To investigate the effect of Pin1/DAPK1/IKK on I/R neuronal cell death, MCAo (Middle cerebral artery occlusion) surgery was performed to experimental animals, and they were injected with either Pin1 inhibitor or DAPK1 inhibitor. The experimental animals were randomly divided into six groups; vehicle‐day1, Pin1 inhibitor‐day1, DAPK1 inhibitor‐day1, vehicle‐day3, Pin1 inhibitor‐day3, DAPK1 inhibitor‐day3. No significant changes were found in the body weight and NDSS scores among groups. However, the inhibition groups exhibited decrease in infarct size and neuronal cell damage after cerebral ischemia/reperfusion. In addition, IKK expression was decreased in inhibition groups. Taken together, regulation of Pin1/DAPK1/IKK interaction would exert neuroprotective effect against I/R injury.Support or Funding InformationNRF‐2013R1A2A2A01067169, NRF‐2017R1A2A2A01067169, KRIBB‐KGM4611714This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.
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