PMID- 23301071 OWN - NLM STAT- MEDLINE DCOM- 20130820 LR - 20231104 IS - 1932-6203 (Electronic) IS - 1932-6203 (Linking) VI - 8 IP - 1 DP - 2013 TI - Hypothermia protects the brain from transient global ischemia/reperfusion by attenuating endoplasmic reticulum response-induced apoptosis through CHOP. PG - e53431 LID - 10.1371/journal.pone.0053431 [doi] LID - e53431 AB - Endoplasmic reticulum (ER) stress has been implicated in the pathology of cerebral ischemia. Apoptotic cell death occurs during prolonged period of stress or when the adaptive response fails. Hypothermia blocked the TNF or Fas-mediated extrinsic apoptosis pathway and the mitochondria pathway of apoptosis, however, whether hypothermia can block endoplasmic reticulum mediated apoptosis is never known. This study aimed to elucidate whether hypothermia attenuates brain cerebral ischemia/reperfusion (I/R) damage by suppressing ER stress-induced apoptosis. A 15 min global cerebral ischemia rat model was used in this study. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) positive cells in hippocampus CA1 were assessed after reperfusion of the brain. The expressions of C/EBP-homologous protein (CHOP) and glucose-regulated protein 78 (GRP78) in ischemic hippocampus CA1 were measured at 6, 12, 24 and 48 h after reperfusion. The results showed that hypothermia significantly attenuated brain I/R injury, as shown by reduction in cell apoptosis, CHOP expression, and increase in GRP78 expression. These results suggest that hypothermia could protect brain from I/R injury by suppressing ER stress-induced apoptosis. FAU - Liu, Xiaojie AU - Liu X AD - Department of Anesthesiology, Qingdao Municipal Hospital, Shandong, China. FAU - Wang, Mingshan AU - Wang M FAU - Chen, Huailong AU - Chen H FAU - Guo, Yunliang AU - Guo Y FAU - Ma, Fuguo AU - Ma F FAU - Shi, Fei AU - Shi F FAU - Bi, Yanlin AU - Bi Y FAU - Li, Ying AU - Li Y LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Retracted Publication DEP - 20130103 PL - United States TA - PLoS One JT - PloS one JID - 101285081 RN - 0 (GRP78 protein, rat) RN - 0 (Heat-Shock Proteins) RN - 147336-12-7 (Transcription Factor CHOP) SB - IM RIN - PLoS One. 2021 Mar 18;16(3):e0249055. PMID: 33735279 MH - Animals MH - *Apoptosis MH - Brain/*metabolism MH - Brain Ischemia/metabolism/pathology MH - Endoplasmic Reticulum/*metabolism MH - Heat-Shock Proteins/metabolism MH - Hippocampus/metabolism MH - *Hypothermia, Induced MH - Immunohistochemistry MH - In Situ Nick-End Labeling MH - Male MH - Mitochondria/metabolism MH - Rats MH - Rats, Wistar MH - Reperfusion Injury/*prevention & control MH - Time Factors MH - Transcription Factor CHOP/*metabolism PMC - PMC3536702 COIS- Competing Interests: The authors have declared that no competing interests exist. EDAT- 2013/01/10 06:00 MHDA- 2013/08/21 06:00 PMCR- 2013/01/03 CRDT- 2013/01/10 06:00 PHST- 2012/08/31 00:00 [received] PHST- 2012/11/28 00:00 [accepted] PHST- 2013/01/10 06:00 [entrez] PHST- 2013/01/10 06:00 [pubmed] PHST- 2013/08/21 06:00 [medline] PHST- 2013/01/03 00:00 [pmc-release] AID - PONE-D-12-27607 [pii] AID - 10.1371/journal.pone.0053431 [doi] PST - ppublish SO - PLoS One. 2013;8(1):e53431. doi: 10.1371/journal.pone.0053431. Epub 2013 Jan 3.