Neural Regeneration Research ›› 2015, Vol. 10 ›› Issue (10): 1604-1611.doi: 10.4103/1673-5374.167757

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Monocarboxylate transporter 4 plays a significant role in the neuroprotective mechanism of ischemic preconditioning in transient cerebral ischemia

Seongkweon Hong1, #, Ji Yun Ahn2, 3, #, Geum-Sil Cho4, In Hye Kim5, Jeong Hwi Cho5, Ji Hyeon Ahn5, Joon Ha Park5, Moo-Ho Won5, Bai Hui Chen6, Bich-Na Shin6, Hyun-Jin Tae7, Seung Min Park2, 3, Jun Hwi Cho3, Soo Young Choi7, *, Jae-Chul Lee5,*   

  1. 1 Department of Surgery, School of Medicine, Kangwon National University, Chuncheon, South Korea
    2 Department of Emergency Medicine, Sacred Heart Hospital, College of Medicine, Hallym University, Anyang, South Korea
    3 Department of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon, South Korea
    4 Department of Neuroscience, College of Medicine, Korea University, Seoul, South Korea
    5 Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea
    6 Department of Physiology, College of Medicine, Hallym University, Chuncheon, South Korea
    7 Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, South Korea
  • Received:2015-08-12 Online:2015-10-28 Published:2015-10-28
  • Contact: Soo Young Choi, Ph.D. or Jae-Chul Lee, Ph.D., sychoi@hallym.ac.kr or anajclee@kangwon.ac.kr.
  • Supported by:

    This work was supported by a Priority Research Centers Program grant (NRF-2009-0093812) through the National Research Foundation of Korea funded by the Ministry of Science, ICT and Future Planning, and by 2014 Research Grant from Kangwon National University

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Abstract:

Monocarboxylate transporters (MCTs), which carry monocarboxylates such as lactate across biological membranes, have been associated with cerebral ischemia/reperfusion process. In this study, we studied the effect of ischemic preconditioning (IPC) on MCT4 immunoreactivity after 5 minutes of transient cerebral ischemia in the gerbil. Animals were randomly designated to four groups (sham-operated group, ischemia only group, IPC + sham-operated group and IPC + ischemia group). A serious loss of neuron was found in the stratum pyramidale of the hippocampal CA1 region (CA1), not CA2/3, of the ischemia-only group at 5 days post-ischemia;
however, in the IPC + ischemia groups, neurons in the stratum pyramidale of the CA1 were well protected. Weak MCT4 immunoreactivity was found in the stratum pyramidale of the CA1 in the sham-operated group. MCT4 immunoreactivity in the stratum pyramidale began to decrease at 2 days post-ischemia and was hardly detected at 5 days post-ischemia; at this time point, MCT4 immunoreactivity was newly expressed in astrocytes. In the IPC + sham-operated group, MCT4 immunoreactivity in the stratum pyramidale of the CA1 was increased compared with the sham-operated group, and, in the IPC + ischemia group, MCT4 immunoreactivity was also increased in the stratum pyramidale compared with the ischemia only group. Briefly, present findings show that IPC apparently protected CA1 pyramidal neurons and increased or maintained
MCT4 expression in the stratum pyramidale of the CA1 after transient cerebral ischemia. Our findings suggest that MCT4 appears to play a significant role in the neuroprotective mechanism
of IPC in the gerbil with transient cerebral ischemia.

Key words: nerve regeneration, monocarboxylate transporters, ischemic preconditioning, ischemia/reperfusion injury, hippocampus, CA1 pyramidal neurons, neural regeneration