The Hypothermic Influence on CHOP and Ero1-α in an Endoplasmic Reticulum Stress Model of Cerebral Ischemia

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The Hypothermic Influence on CHOP and Ero1-α in an Endoplasmic Reticulum Stress Model of Cerebral Ischemia. / Poone, Gagandip K.; Hasseldam, Henrik; Munkholm, Nina; Rasmussen, Rune S.; Grønberg, Nina V.; Johansen, Flemming Fryd.

In: Brain Sciences, Vol. 5, 15.05.2015, p. 178-187.

Research output: Contribution to journalJournal articleResearchpeer-review

Harvard

Poone, GK, Hasseldam, H, Munkholm, N, Rasmussen, RS, Grønberg, NV & Johansen, FF 2015, 'The Hypothermic Influence on CHOP and Ero1-α in an Endoplasmic Reticulum Stress Model of Cerebral Ischemia', Brain Sciences, vol. 5, pp. 178-187. https://doi.org/10.3390/brainsci5020178

APA

Poone, G. K., Hasseldam, H., Munkholm, N., Rasmussen, R. S., Grønberg, N. V., & Johansen, F. F. (2015). The Hypothermic Influence on CHOP and Ero1-α in an Endoplasmic Reticulum Stress Model of Cerebral Ischemia. Brain Sciences, 5, 178-187. https://doi.org/10.3390/brainsci5020178

Vancouver

Poone GK, Hasseldam H, Munkholm N, Rasmussen RS, Grønberg NV, Johansen FF. The Hypothermic Influence on CHOP and Ero1-α in an Endoplasmic Reticulum Stress Model of Cerebral Ischemia. Brain Sciences. 2015 May 15;5:178-187. https://doi.org/10.3390/brainsci5020178

Author

Poone, Gagandip K. ; Hasseldam, Henrik ; Munkholm, Nina ; Rasmussen, Rune S. ; Grønberg, Nina V. ; Johansen, Flemming Fryd. / The Hypothermic Influence on CHOP and Ero1-α in an Endoplasmic Reticulum Stress Model of Cerebral Ischemia. In: Brain Sciences. 2015 ; Vol. 5. pp. 178-187.

Bibtex

@article{3fe6840917404d77b3a714381cbed40d,
title = "The Hypothermic Influence on CHOP and Ero1-α in an Endoplasmic Reticulum Stress Model of Cerebral Ischemia",
abstract = "Hypoxia induced endoplasmic reticulum stress causes accumulation of unfolded proteins in the endoplasmic reticulum and activates the unfolded protein response,resulting in apoptosis through CCAAT-enhancer-binding protein homologous protein (CHOP) activation. In an in vitro and in vivo model of ischemic stroke, we investigated whether hypothermia regulates the unfolded protein response of CHOP and Endoplas micreticulum oxidoreductin-α (Ero1-α), because Ero1-α is suggested to be a downstream CHOP target. The gene expression of CHOP and Ero1-α was measured using Quantitative-PCR (Q-PCR) in rat hippocampi following global cerebral ischemia, and inhypoxic pheochromocytoma cells during normothermic (37 °C) and hypothermic (31 °C)conditions. As a result of ischemia, a significant increase in expression of CHOP andEro1-α was observed after three, six and twelve hours of reperfusion following globalischemia. A stable increase in CHOP expression was observed throughout the time course (p < 0.01, p < 0.0001), whereas Ero1-α expression peaked at three to six hours (p < 0.0001). Induced hypothermia in hypoxia stressed PC12 cells resulted in a decreased expression of CHOP after three, six and twelve hours (p < 0.0001). On the contrary, thegene expression of Ero1-α increased as a result of hypothermia and peaked at twelve hours (p < 0.0001). Hypothermia attenuated the expression of CHOP, supporting that hypothermia suppress endoplasmic reticulum stress induced apoptosis in stroke. Ashypothermia further induced up-regulation of Ero1-α, and since CHOP and Ero1-α showed differential regulation as a consequence of both disease (hypoxia) and treatment (hypothermia), we conclude that they are regulated independently.",
keywords = "Faculty of Health and Medical Sciences",
author = "Poone, {Gagandip K.} and Henrik Hasseldam and Nina Munkholm and Rasmussen, {Rune S.} and Gr{\o}nberg, {Nina V.} and Johansen, {Flemming Fryd}",
year = "2015",
month = "5",
day = "15",
doi = "10.3390/brainsci5020178",
language = "English",
volume = "5",
pages = "178--187",
journal = "Brain Sciences",
issn = "2076-3425",
publisher = "M D P I AG",

}

RIS

TY - JOUR

T1 - The Hypothermic Influence on CHOP and Ero1-α in an Endoplasmic Reticulum Stress Model of Cerebral Ischemia

AU - Poone, Gagandip K.

AU - Hasseldam, Henrik

AU - Munkholm, Nina

AU - Rasmussen, Rune S.

AU - Grønberg, Nina V.

AU - Johansen, Flemming Fryd

PY - 2015/5/15

Y1 - 2015/5/15

N2 - Hypoxia induced endoplasmic reticulum stress causes accumulation of unfolded proteins in the endoplasmic reticulum and activates the unfolded protein response,resulting in apoptosis through CCAAT-enhancer-binding protein homologous protein (CHOP) activation. In an in vitro and in vivo model of ischemic stroke, we investigated whether hypothermia regulates the unfolded protein response of CHOP and Endoplas micreticulum oxidoreductin-α (Ero1-α), because Ero1-α is suggested to be a downstream CHOP target. The gene expression of CHOP and Ero1-α was measured using Quantitative-PCR (Q-PCR) in rat hippocampi following global cerebral ischemia, and inhypoxic pheochromocytoma cells during normothermic (37 °C) and hypothermic (31 °C)conditions. As a result of ischemia, a significant increase in expression of CHOP andEro1-α was observed after three, six and twelve hours of reperfusion following globalischemia. A stable increase in CHOP expression was observed throughout the time course (p < 0.01, p < 0.0001), whereas Ero1-α expression peaked at three to six hours (p < 0.0001). Induced hypothermia in hypoxia stressed PC12 cells resulted in a decreased expression of CHOP after three, six and twelve hours (p < 0.0001). On the contrary, thegene expression of Ero1-α increased as a result of hypothermia and peaked at twelve hours (p < 0.0001). Hypothermia attenuated the expression of CHOP, supporting that hypothermia suppress endoplasmic reticulum stress induced apoptosis in stroke. Ashypothermia further induced up-regulation of Ero1-α, and since CHOP and Ero1-α showed differential regulation as a consequence of both disease (hypoxia) and treatment (hypothermia), we conclude that they are regulated independently.

AB - Hypoxia induced endoplasmic reticulum stress causes accumulation of unfolded proteins in the endoplasmic reticulum and activates the unfolded protein response,resulting in apoptosis through CCAAT-enhancer-binding protein homologous protein (CHOP) activation. In an in vitro and in vivo model of ischemic stroke, we investigated whether hypothermia regulates the unfolded protein response of CHOP and Endoplas micreticulum oxidoreductin-α (Ero1-α), because Ero1-α is suggested to be a downstream CHOP target. The gene expression of CHOP and Ero1-α was measured using Quantitative-PCR (Q-PCR) in rat hippocampi following global cerebral ischemia, and inhypoxic pheochromocytoma cells during normothermic (37 °C) and hypothermic (31 °C)conditions. As a result of ischemia, a significant increase in expression of CHOP andEro1-α was observed after three, six and twelve hours of reperfusion following globalischemia. A stable increase in CHOP expression was observed throughout the time course (p < 0.01, p < 0.0001), whereas Ero1-α expression peaked at three to six hours (p < 0.0001). Induced hypothermia in hypoxia stressed PC12 cells resulted in a decreased expression of CHOP after three, six and twelve hours (p < 0.0001). On the contrary, thegene expression of Ero1-α increased as a result of hypothermia and peaked at twelve hours (p < 0.0001). Hypothermia attenuated the expression of CHOP, supporting that hypothermia suppress endoplasmic reticulum stress induced apoptosis in stroke. Ashypothermia further induced up-regulation of Ero1-α, and since CHOP and Ero1-α showed differential regulation as a consequence of both disease (hypoxia) and treatment (hypothermia), we conclude that they are regulated independently.

KW - Faculty of Health and Medical Sciences

U2 - 10.3390/brainsci5020178

DO - 10.3390/brainsci5020178

M3 - Journal article

C2 - 25989620

VL - 5

SP - 178

EP - 187

JO - Brain Sciences

JF - Brain Sciences

SN - 2076-3425

ER -

ID: 137657017