RbAp48 expression and neuronal damage in the gerbil hippocampus following 5 min of transient ischemia

Joon Ha Park; Tae-Kyeong Lee; Dae Won Kim; Cheol Woo Park; Young Eun Park; Bora Kim; Jae-Chul Lee; Hyang-Ah Lee; Moo-Ho Won; Ji Hyeon Ahn

doi:10.1186/s42826-019-0011-3

RbAp48 expression and neuronal damage in the gerbil hippocampus following 5 min of transient ischemia

Lab Anim Res. 2019 Jul 31:35:12. doi: 10.1186/s42826-019-0011-3. eCollection 2019.

Authors

Affiliations

¹ 1Department of Biomedical Science, Research Institute of Bioscience and Biotechnology, Hallym University, Chuncheon, Gangwon 24252 Republic of Korea.
² 2Department of Neurobiology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 24341 Republic of Korea.
³ Department of Biochemistry and Molecular Biology, and Research Institute of Oral Sciences, College of Dentistry, Gangnung-Wonju National University, Gangneung, Gangwon 25457 Republic of Korea.
⁴ 4Department of Obstetrics and Gynecology, School of Medicine, Kangwon National University, Chuncheon, Gangwon 24341 Republic of Korea.

^# Contributed equally.

Abstract

Histone-binding protein RbAp48 has been known to be involved in histone acetylation, and epigenetic alterations of histone modifications are closely associated with the pathogenesis of ischemic reperfusion injury. In the current study, we investigated chronological change of RbAp48 expression in the hippocampus following 5 min of transient ischemia in gerbils. RbAp48 expression was examined 1, 2, 5, and 10 days after transient ischemia using immunohistochemistry. In sham operated gerbils, RbAp48 immunoreactivity was strong in pyramidal and non-pyramidal cells in the hippocampus. After transient ischemia, RbAp48 immunoreactivity was changed in the cornu ammonis 1 subfield (CA1), not in CA2/3. RbAp48 immunoreactivity in CA1 pyramidal neurons was gradually decreased and not detected at 5 and 10 days after ischemia. RbAp48 immunoreactivity in non-pyramidal cells was maintained until 2 days post-ischemia and significantly increased from 5 days post-ischemia. Double immunohistofluorescence staining revealed that RbAp48 immunoreactive non-pyramidal cells were astrocytes. At 5 days post-ischemia, death of pyramidal neurons occurred only in the CA1. These results showed that RbAp48 immunoreactivity was distinctively altered in pyramidal neurons and astrocytes in the hippocampal CA1 following 5 mins of transient ischemia. Ischemia-induced change in RbAp48 expression may be closely associated with neuronal death and astrocyte activation following 5 min of transient ischemia.

Keywords: Astrocytes activation, delayed neuronal death; RbAp48; Transient ischemia.