Pretreatment with apoaequorin protects hippocampal CA1 neurons from oxygen-glucose deprivation.

Ischemic stroke affects ∼795,000 people each year in the U.S., which results in an estimated annual cost of $73.7 billion. Calcium is pivotal in a variety of neuronal signaling cascades, however, during ischemia, excess calcium influx can trigger excitotoxic cell death. Calcium binding proteins help...

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Autores principales:	Julia A Detert, Erin L Adams, Jacob D Lescher, Jeri-Anne Lyons, James R Moyer
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/af88263b7ce54a9ab905327b900cac30
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spelling	oai:doaj.org-article:af88263b7ce54a9ab905327b900cac302021-11-18T08:47:28ZPretreatment with apoaequorin protects hippocampal CA1 neurons from oxygen-glucose deprivation.1932-620310.1371/journal.pone.0079002https://doaj.org/article/af88263b7ce54a9ab905327b900cac302013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24244400/?tool=EBIhttps://doaj.org/toc/1932-6203Ischemic stroke affects ∼795,000 people each year in the U.S., which results in an estimated annual cost of $73.7 billion. Calcium is pivotal in a variety of neuronal signaling cascades, however, during ischemia, excess calcium influx can trigger excitotoxic cell death. Calcium binding proteins help neurons regulate/buffer intracellular calcium levels during ischemia. Aequorin is a calcium binding protein isolated from the jellyfish Aequorea victoria, and has been used for years as a calcium indicator, but little is known about its neuroprotective properties. The present study used an in vitro rat brain slice preparation to test the hypothesis that an intra-hippocampal infusion of apoaequorin (the calcium binding component of aequorin) protects neurons from ischemic cell death. Bilaterally cannulated rats received an apoaequorin infusion in one hemisphere and vehicle control in the other. Hippocampal slices were then prepared and subjected to 5 minutes of oxygen-glucose deprivation (OGD), and cell death was assayed by trypan blue exclusion. Apoaequorin dose-dependently protected neurons from OGD--doses of 1% and 4% (but not 0.4%) significantly decreased the number of trypan blue-labeled neurons. This effect was also time dependent, lasting up to 48 hours. This time dependent effect was paralleled by changes in cytokine and chemokine expression, indicating that apoaequorin may protect neurons via a neuroimmunomodulatory mechanism. These data support the hypothesis that pretreatment with apoaequorin protects neurons against ischemic cell death, and may be an effective neurotherapeutic.Julia A DetertErin L AdamsJacob D LescherJeri-Anne LyonsJames R MoyerPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 11, p e79002 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Julia A Detert Erin L Adams Jacob D Lescher Jeri-Anne Lyons James R Moyer Pretreatment with apoaequorin protects hippocampal CA1 neurons from oxygen-glucose deprivation.
description	Ischemic stroke affects ∼795,000 people each year in the U.S., which results in an estimated annual cost of $73.7 billion. Calcium is pivotal in a variety of neuronal signaling cascades, however, during ischemia, excess calcium influx can trigger excitotoxic cell death. Calcium binding proteins help neurons regulate/buffer intracellular calcium levels during ischemia. Aequorin is a calcium binding protein isolated from the jellyfish Aequorea victoria, and has been used for years as a calcium indicator, but little is known about its neuroprotective properties. The present study used an in vitro rat brain slice preparation to test the hypothesis that an intra-hippocampal infusion of apoaequorin (the calcium binding component of aequorin) protects neurons from ischemic cell death. Bilaterally cannulated rats received an apoaequorin infusion in one hemisphere and vehicle control in the other. Hippocampal slices were then prepared and subjected to 5 minutes of oxygen-glucose deprivation (OGD), and cell death was assayed by trypan blue exclusion. Apoaequorin dose-dependently protected neurons from OGD--doses of 1% and 4% (but not 0.4%) significantly decreased the number of trypan blue-labeled neurons. This effect was also time dependent, lasting up to 48 hours. This time dependent effect was paralleled by changes in cytokine and chemokine expression, indicating that apoaequorin may protect neurons via a neuroimmunomodulatory mechanism. These data support the hypothesis that pretreatment with apoaequorin protects neurons against ischemic cell death, and may be an effective neurotherapeutic.
format	article
author	Julia A Detert Erin L Adams Jacob D Lescher Jeri-Anne Lyons James R Moyer
author_facet	Julia A Detert Erin L Adams Jacob D Lescher Jeri-Anne Lyons James R Moyer
author_sort	Julia A Detert
title	Pretreatment with apoaequorin protects hippocampal CA1 neurons from oxygen-glucose deprivation.
title_short	Pretreatment with apoaequorin protects hippocampal CA1 neurons from oxygen-glucose deprivation.
title_full	Pretreatment with apoaequorin protects hippocampal CA1 neurons from oxygen-glucose deprivation.
title_fullStr	Pretreatment with apoaequorin protects hippocampal CA1 neurons from oxygen-glucose deprivation.
title_full_unstemmed	Pretreatment with apoaequorin protects hippocampal CA1 neurons from oxygen-glucose deprivation.
title_sort	pretreatment with apoaequorin protects hippocampal ca1 neurons from oxygen-glucose deprivation.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/af88263b7ce54a9ab905327b900cac30
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Pretreatment with apoaequorin protects hippocampal CA1 neurons from oxygen-glucose deprivation.

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