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Galectin-3 expression in hippocampal CA2 following transient forebrain ischemia and its inhibition by hypothermia or antiapoptotic agents

Recent evidence has suggested that the hippocampal CA2 region plays an important role in the recognition process. We have reported that ischemic damage in the hippocampal CA2 region following transient ischemia is caused by apoptosis, but the underlying mechanisms are still not clear. Galectin-3 is...

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Autores principales: Hisamatsu, Kenji, Niwa, Masayuki, Kobayashi, Kazuhiro, Miyazaki, Tatsuhiko, Hirata, Akihiro, Hatano, Yuichiro, Tomita, Hiroyuki, Hara, Akira
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4782821/
https://www.ncbi.nlm.nih.gov/pubmed/26848998
http://dx.doi.org/10.1097/WNR.0000000000000538
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author Hisamatsu, Kenji
Niwa, Masayuki
Kobayashi, Kazuhiro
Miyazaki, Tatsuhiko
Hirata, Akihiro
Hatano, Yuichiro
Tomita, Hiroyuki
Hara, Akira
author_facet Hisamatsu, Kenji
Niwa, Masayuki
Kobayashi, Kazuhiro
Miyazaki, Tatsuhiko
Hirata, Akihiro
Hatano, Yuichiro
Tomita, Hiroyuki
Hara, Akira
author_sort Hisamatsu, Kenji
collection PubMed
description Recent evidence has suggested that the hippocampal CA2 region plays an important role in the recognition process. We have reported that ischemic damage in the hippocampal CA2 region following transient ischemia is caused by apoptosis, but the underlying mechanisms are still not clear. Galectin-3 is a β-galactosidase-binding lectin that is important in cell proliferation and apoptotic regulation. We have also reported that galectin-3 was expressed in activated microglia in the CA1 region 96 h after transient ischemia. The aim of this study is to determine the localization and time course of galectin-3 expression in the CA2 region following transient forebrain ischemia. Galectin-3 immunostaining was observed in both interior side of CA1 region and CA2 region in hippocampus 60 h after ischemic insult. At 66 h, galectin-3 was observed in the whole CA1 region adjacent to the CA2 region in the hippocampus. Both galectin-3 expression and neuronal cell death in the CA2 region were significantly inhibited by hypothermia and by apoptosis-inhibiting reagents. These results suggest that galectin-3 in the CA2 region is expressed independent of that in the CA1 region. Protection of the expression of galectin-3 in the CA2 region might contribute toward the survival of CA2 pyramidal neurons.
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spelling pubmed-47828212016-03-28 Galectin-3 expression in hippocampal CA2 following transient forebrain ischemia and its inhibition by hypothermia or antiapoptotic agents Hisamatsu, Kenji Niwa, Masayuki Kobayashi, Kazuhiro Miyazaki, Tatsuhiko Hirata, Akihiro Hatano, Yuichiro Tomita, Hiroyuki Hara, Akira Neuroreport Degeneration and Repair Recent evidence has suggested that the hippocampal CA2 region plays an important role in the recognition process. We have reported that ischemic damage in the hippocampal CA2 region following transient ischemia is caused by apoptosis, but the underlying mechanisms are still not clear. Galectin-3 is a β-galactosidase-binding lectin that is important in cell proliferation and apoptotic regulation. We have also reported that galectin-3 was expressed in activated microglia in the CA1 region 96 h after transient ischemia. The aim of this study is to determine the localization and time course of galectin-3 expression in the CA2 region following transient forebrain ischemia. Galectin-3 immunostaining was observed in both interior side of CA1 region and CA2 region in hippocampus 60 h after ischemic insult. At 66 h, galectin-3 was observed in the whole CA1 region adjacent to the CA2 region in the hippocampus. Both galectin-3 expression and neuronal cell death in the CA2 region were significantly inhibited by hypothermia and by apoptosis-inhibiting reagents. These results suggest that galectin-3 in the CA2 region is expressed independent of that in the CA1 region. Protection of the expression of galectin-3 in the CA2 region might contribute toward the survival of CA2 pyramidal neurons. Lippincott Williams & Wilkins 2016-03-23 2016-03-09 /pmc/articles/PMC4782821/ /pubmed/26848998 http://dx.doi.org/10.1097/WNR.0000000000000538 Text en Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. This is an open-access article distributed under the terms of the Creative Commons Attribution-Non Commercial-No Derivatives License 4.0 (CCBY-NC-ND), where it is permissible to download and share the work provided it is properly cited. The work cannot be changed in any way or used commercially. http://creativecommons.org/licenses/by-nc-nd/4.0/
spellingShingle Degeneration and Repair
Hisamatsu, Kenji
Niwa, Masayuki
Kobayashi, Kazuhiro
Miyazaki, Tatsuhiko
Hirata, Akihiro
Hatano, Yuichiro
Tomita, Hiroyuki
Hara, Akira
Galectin-3 expression in hippocampal CA2 following transient forebrain ischemia and its inhibition by hypothermia or antiapoptotic agents
title Galectin-3 expression in hippocampal CA2 following transient forebrain ischemia and its inhibition by hypothermia or antiapoptotic agents
title_full Galectin-3 expression in hippocampal CA2 following transient forebrain ischemia and its inhibition by hypothermia or antiapoptotic agents
title_fullStr Galectin-3 expression in hippocampal CA2 following transient forebrain ischemia and its inhibition by hypothermia or antiapoptotic agents
title_full_unstemmed Galectin-3 expression in hippocampal CA2 following transient forebrain ischemia and its inhibition by hypothermia or antiapoptotic agents
title_short Galectin-3 expression in hippocampal CA2 following transient forebrain ischemia and its inhibition by hypothermia or antiapoptotic agents
title_sort galectin-3 expression in hippocampal ca2 following transient forebrain ischemia and its inhibition by hypothermia or antiapoptotic agents
topic Degeneration and Repair
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4782821/
https://www.ncbi.nlm.nih.gov/pubmed/26848998
http://dx.doi.org/10.1097/WNR.0000000000000538
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