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Neural Regen Res. 2015 Jun;10(6):944-50. doi: 10.4103/1673-5374.158359.

Delayed hippocampal neuronal death in young gerbil following transient global cerebral ischemia is related to higher and longer-term expression of p63 in the ischemic hippocampus.

Neural regeneration research

Eun Joo Bae, Bai Hui Chen, Bing Chun Yan, Bich Na Shin, Jeong Hwi Cho, In Hye Kim, Ji Hyeon Ahn, Jae Chul Lee, Hyun-Jin Tae, Seongkweon Hong, Dong Won Kim, Jun Hwi Cho, Yun Lyul Lee, Moo-Ho Won, Joon Ha Park

Affiliations

  1. Department of Pediatrics, Chuncheon Sacred Heart Hospital, College of Medicine, Hallym University, Chuncheon, South Korea.
  2. Department of Physiology, College of Medicine, Institute of Neurodegeneration and Neuroregeneration, Hallym University, Chuncheon, South Korea.
  3. Institute of Integrative Traditional & Western Medicine, Medical College, Yangzhou University, Yangzhou, Jiangsu Province, China.
  4. Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea.
  5. Department of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University, Chunchon, South Korea.
  6. Department of Surgery, School of Medicine, Kangwon National University, Chuncheon, South Korea.
  7. Department of Emergency Medicine, Chuncheon Sacred Heart Hospital, College of Medicine, Hallym University, Chuncheon, South Korea ; Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, South Korea.
  8. Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, South Korea.

PMID: 26199612 PMCID: PMC4498357 DOI: 10.4103/1673-5374.158359

Abstract

The tumor suppressor p63 is one of p53 family members and plays a vital role as a regulator of neuronal apoptosis in the development of the nervous system. However, the role of p63 in mature neuronal death has not been addressed yet. In this study, we first compared ischemia-induced effects on p63 expression in the hippocampal regions (CA1-3) between the young and adult gerbils subjected to 5 minutes of transient global cerebral ischemia. Neuronal death in the hippocampal CA1 region of young gerbils was significantly slow compared with that in the adult gerbils after transient global cerebral ischemia. p63 immunoreactivity in the hippocampal CA1 pyramidal neurons in the sham-operated young group was significantly low compared with that in the sham-operated adult group. p63 immunoreactivity was apparently changed in ischemic hippocampal CA1 pyramidal neurons in both ischemia-operated young and adult groups. In the ischemia-operated adult groups, p63 immunoreactivity in the hippocampal CA1 pyramidal neurons was significantly decreased at 4 days post-ischemia; however, p63 immunoreactivity in the ischemia-operated young group was significantly higher than that in the ischemia-operated adult group. At 7 days post-ischemia, p63 immunoreactivity was decreased in the hippocampal CA1 pyramidal neurons in both ischemia-operated young and adult groups. Change patterns of p63 level in the hippocampal CA1 region of adult and young gerbils after ischemic damage were similar to those observed in the immunohistochemical results. These findings indicate that higher and longer-term expression of p63 in the hippocampal CA1 region of the young gerbils after ischemia/reperfusion may be related to more delayed neuronal death compared to that in the adults.

Keywords: CA1 region; cerebral ischemia/reperfusion; delayed neuronal death; immunohistochemistry; neural regeneration; p53 tumor suppressor gene family; pyramidal neurons; western blotting

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