{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T02:48:31Z","timestamp":1792464511036,"version":"4.5.0"},"reference-count":32,"publisher":"SAGE Publications","issue":"4","license":[{"start":{"date-parts":[[2017,8,4]],"date-time":"2017-08-04T00:00:00Z","timestamp":1501804800000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["International Journal of Stroke"],"published-print":{"date-parts":[[2018,6]]},"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Cornu ammonis 3 (CA3) hippocampal neurons are resistant to global ischemia, whereas cornu ammonis (CA1) 1 neurons are vulnerable. Hamartin expression in CA3 neurons mediates this endogenous resistance via productive autophagy. Neurons lacking hamartin demonstrate exacerbated endoplasmic reticulum stress and increased cell death. We investigated endoplasmic reticulum stress responses in CA1 and CA3 regions following global cerebral ischemia, and whether pharmacological modulation of endoplasmic reticulum stress or autophagy altered neuronal viability .<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>In\u00a0vivo: male Wistar rats underwent sham or 10 min of transient global cerebral ischemia. CA1 and CA3 areas were microdissected and endoplasmic reticulum stress protein expression quantified at 3\u2009h and 12\u2009h of reperfusion. In\u00a0vitro: primary neuronal cultures (E18 Wistar rat embryos) were exposed to 2\u2009h of oxygen and glucose deprivation or normoxia in the presence of an endoplasmic reticulum stress inducer (thapsigargin or tunicamycin), an endoplasmic reticulum stress inhibitor (salubrinal or 4-phenylbutyric acid), an autophagy inducer ([4\u2032-(N-diethylamino) butyl]-2-chlorophenoxazine (10-NCP)) or autophagy inhibitor (3-methyladenine).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>In\u00a0vivo, decreased endoplasmic reticulum stress protein expression (phospho-eIF2\u03b1 and ATF4) was observed at 3\u2009h of reperfusion in CA3 neurons following ischemia, and increased in CA1 neurons at 12\u2009h of reperfusion. In\u00a0vitro, endoplasmic reticulum stress inducers and high doses of the endoplasmic reticulum stress inhibitors also increased cell death. Both induction and inhibition of autophagy also increased cell death.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Endoplasmic reticulum stress is associated with neuronal cell death following ischemia. Neither reduction of endoplasmic reticulum stress nor induction of autophagy demonstrated neuroprotection in\u00a0vitro, highlighting their complex role in neuronal biology following ischemia.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1177\/1747493017724584","type":"journal-article","created":{"date-parts":[[2017,8,4]],"date-time":"2017-08-04T07:06:38Z","timestamp":1501830398000},"page":"379-390","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":37,"title":["The role of the endoplasmic reticulum stress response following cerebral ischemia"],"prefix":"10.1177","volume":"13","author":[{"given":"Gina","family":"Hadley","sequence":"first","affiliation":[{"name":"Acute Stroke Programme, Radcliffe Department of Medicine, University of Oxford, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ain A","family":"Neuhaus","sequence":"additional","affiliation":[{"name":"Acute Stroke Programme, Radcliffe Department of Medicine, University of Oxford, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yvonne","family":"Couch","sequence":"additional","affiliation":[{"name":"Acute Stroke Programme, Radcliffe Department of Medicine, University of Oxford, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel J","family":"Beard","sequence":"additional","affiliation":[{"name":"Acute Stroke Programme, Radcliffe Department of Medicine, University of Oxford, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bryan A","family":"Adriaanse","sequence":"additional","affiliation":[{"name":"Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kostas","family":"Vekrellis","sequence":"additional","affiliation":[{"name":"Department of Neuroscience, Center for Basic Research, Biomedical Research Foundation of the Academy of Athens, Athens, Greece"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gabriele C","family":"DeLuca","sequence":"additional","affiliation":[{"name":"Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michalis","family":"Papadakis","sequence":"additional","affiliation":[{"name":"Acute Stroke Programme, Radcliffe Department of Medicine, University of Oxford, Oxford, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brad A","family":"Sutherland","sequence":"additional","affiliation":[{"name":"Acute Stroke Programme, Radcliffe Department of Medicine, University of Oxford, Oxford, UK"},{"name":"School of Medicine, Faculty of Health, University of Tasmania, Hobart, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alastair M","family":"Buchan","sequence":"additional","affiliation":[{"name":"Acute Stroke Programme, Radcliffe Department of 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