Neural Regeneration Research ›› 2016, Vol. 11 ›› Issue (6): 924-930.doi: 10.4103/1673-5374.184490

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Time- and cell-type specific changes in iron, ferritin, and transferrin in the gerbil hippocampal CA1 region after transient forebrain ischemia

Dae Young Yoo1, Ki-Yeon Yoo2, Joon Ha Park3, Hyun Jung Kwon4, Hyo Young Jung1, Jong Whi Kim1, Goang-Min Choi5, Seung Myung Moon6, Dae Won Kim4, Yeo Sung Yoon1, Moo-Ho Won3, In Koo Hwang1, *   

  1. 1 Department of Anatomy and Cell Biology, College of Veterinary Medicine, and Research Institute for Veterinary Science, Seoul National University, Seoul, South Korea 2 Department of Oral Anatomy, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University, Gangneung, South Korea 3 Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, South Korea 4 Department of Biochemistry and Molecular Biology, Research Institute of Oral Sciences, College of Dentistry, Gangneung-Wonju National University, Gangneung, South Korea 5 Department of Thoracic and Cardiovascular Surgery, Chuncheon Sacred Heart Hospital, College of Medicine, Hallym University, Chuncheon, South Korea 6 Department of Neurosurgery, Dongtan Sacred Heart Hospital, College of Medicine, Hallym University, Hwaseong, South Korea
  • Received:2016-04-28 Online:2016-06-30 Published:2016-06-30
  • Contact: In Koo Hwang, D.V.M., Ph.D., vetmed2@snu.ac.kr.
  • Supported by:

    This work was supported by Basic Science Research Program through the National Research Foundation of Korea (NRF) funded by the Ministry of Education, No. 2015R1D1A1A01059980. This study was also partially supported by the Research Institute for Veterinary Science, Seoul National University.

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Abstract:

In the present study, we used immunohistochemistry and western blot analysis to examine changes in the levels and cellular localization of iron, heavy chain ferritin (ferritin-H), and transferrin in the gerbil hippocampal CA1 region from 30 minutes to 7 days following transient forebrain ischemia. Relative to sham controls, iron reactivity increased significantly in the stratum pyramidale and stratum oriens at 12 hours following ischemic insult, transiently decreased at 1–2 days and then increased once again within the CA1 region at 4–7 days after ischemia. One day after ischemia, ferritin-H immunoreactivity increased significantly in the stratum pyramidale and decreased at 2 days. At 4–7 days after ischemia, ferritin-H immunoreactivity in the glial components in the CA1 region was significantly increased. Transferrin immunoreactivity was increased significantly in the stratum pyramidale at 12 hours, peaked at 1 day, and then decreased significantly at 2 days after ischemia. Seven days after ischemia, Transferrin immunoreactivity in the glial cells of the stratum oriens and radiatum was significantly increased. Western blot analyses supported these results, demonstrating that compared to sham controls, ferritin H and transferrin protein levels in hippocampal homogenates significantly increased at 1 day after ischemia, peaked at 4 days and then decreased. These results suggest that iron overload-induced oxidative stress is most prominent at 12 hours after ischemia in the stratum pyramidale, suggesting that this time window may be the optimal period for therapeutic intervention to protect neurons from ischemia-induced death.

Key words: nerve regeneration, ischemia, iron, ferritin heavy chain, transferrin, CA1 region, oxidative stress, neural regeneration