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Enhancement of neural regeneration and functional recovery via DAPK1 suppression in stroke animal model
Author(s) -
Won Jinyoung,
Hong Yonggeun
Publication year - 2016
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.30.1_supplement.lb630
Subject(s) - neurogenesis , neuroprotection , regeneration (biology) , stroke (engine) , neuroscience , synapse , biology , medicine , microbiology and biotechnology , mechanical engineering , engineering
Stroke is the most frequent worldwide cause of adult death. Recently, studies reported an intimate relation between DAPK1 as key player in multiple cell death and ischemic brain injury. We investigated the effect of DAPK1 on neural regeneration and functional recovery following ischemic injury using by Oxazolone, a synthesized DAPK inhibitor. In ischemic stroke model, subjected animals exhibited neurologic damage and altered behavioral outcome. However, suppression of DAPK1 enhanced neural regeneration and functional recovery. To analysis of neuronal morphology including soma, synapse number, and synaptic recruitment, Golgi‐cox staining was performed. Suppression of DAPK1 induced loss of dendrites length and spine density of pyramidal neurons, and supported progressive improvement of neurological deficits compared to control (P < 0.05). In addition, we investigate whether brain injury was accompanied by changes in levels of BDNF. Expression of immature precursor pro‐BDNF, involved in neuronal apoptosis, was decreased in response to ischemic injury under DAPK inhibited condition (P < 0.05). These results indicate that activation of DAPK1 following the ischemic insult exclusively correlate with brain injury and involve disturbed neurogenesis. Therefore, regulation of downstream molecules in DAPK1 pathway induces neural protection against stroke. Support or Funding Information Funding: NRF‐2012R1A1A2005089, NRF‐2013R1A2A2A01067169