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Article: Selective astrocytic endothelin-1 overexpression contributes to dementia associated with ischemic stroke by exaggerating astrocyte-derived amyloid secretion

TitleSelective astrocytic endothelin-1 overexpression contributes to dementia associated with ischemic stroke by exaggerating astrocyte-derived amyloid secretion
Authors
Issue Date2015
Citation
Journal of Cerebral Blood Flow & Metabolism, 2015, v. 35, p. 1687-1696 How to Cite?
AbstractEndothelin-1 (ET-1) is synthesized by endothelial cells and astrocytes in stroke and in brains of Alzheimer’s disease patients. Our transgenic mice with ET-1 overexpression in the endothelial cells (TET-1) showed more severe blood–brain barrier (BBB) breakdown, neuronal apoptosis, and glial reactivity after 2-hour transient middle cerebral artery occlusion (tMCAO) with 22-hour reperfusion and more severe cognitive deficits after 30 minutes tMCAO with 5 months reperfusion. However, the role of astrocytic ET-1 in contributing to poststroke cognitive deficits after tMCAO is largely unknown. Therefore, GET-1 mice were challenged with tMCAO to determine its effect on neurologic and cognitive deficit. The GET-1 mice transiently displayed a sensorimotor deficit after reperfusion that recovered shortly, then more severe deficit in spatial learning and memory was observed at 3 months after ischemia compared with that of the controls. Upregulation of TNF-α, cleaved caspase-3, and Thioflavin-S-positive aggregates was observed in the ipsilateral hemispheres of the GET-1 brains as early as 3 days after ischemia. In an in vitro study, ET-1 overexpressing astrocytic cells showed amyloid secretion after hypoxia/ischemia insult, which activated endothelin A (ETA) and endothelin B (ETB) receptors in a PI3K/AKT-dependent manner, suggesting role of astrocytic ET-1 in dementia associated with stroke by astrocytederived amyloid production.
Persistent Identifierhttp://hdl.handle.net/10722/218637

 

DC FieldValueLanguage
dc.contributor.authorHung, KL-
dc.contributor.authorYeung, PKK-
dc.contributor.authorLai, KW-
dc.contributor.authorLo, ACY-
dc.contributor.authorChan, CK-
dc.contributor.authorWu, EX-
dc.contributor.authorChung, SM-
dc.contributor.authorChung, SK-
dc.date.accessioned2015-09-18T06:48:53Z-
dc.date.available2015-09-18T06:48:53Z-
dc.date.issued2015-
dc.identifier.citationJournal of Cerebral Blood Flow & Metabolism, 2015, v. 35, p. 1687-1696-
dc.identifier.urihttp://hdl.handle.net/10722/218637-
dc.description.abstractEndothelin-1 (ET-1) is synthesized by endothelial cells and astrocytes in stroke and in brains of Alzheimer’s disease patients. Our transgenic mice with ET-1 overexpression in the endothelial cells (TET-1) showed more severe blood–brain barrier (BBB) breakdown, neuronal apoptosis, and glial reactivity after 2-hour transient middle cerebral artery occlusion (tMCAO) with 22-hour reperfusion and more severe cognitive deficits after 30 minutes tMCAO with 5 months reperfusion. However, the role of astrocytic ET-1 in contributing to poststroke cognitive deficits after tMCAO is largely unknown. Therefore, GET-1 mice were challenged with tMCAO to determine its effect on neurologic and cognitive deficit. The GET-1 mice transiently displayed a sensorimotor deficit after reperfusion that recovered shortly, then more severe deficit in spatial learning and memory was observed at 3 months after ischemia compared with that of the controls. Upregulation of TNF-α, cleaved caspase-3, and Thioflavin-S-positive aggregates was observed in the ipsilateral hemispheres of the GET-1 brains as early as 3 days after ischemia. In an in vitro study, ET-1 overexpressing astrocytic cells showed amyloid secretion after hypoxia/ischemia insult, which activated endothelin A (ETA) and endothelin B (ETB) receptors in a PI3K/AKT-dependent manner, suggesting role of astrocytic ET-1 in dementia associated with stroke by astrocytederived amyloid production.-
dc.languageeng-
dc.relation.ispartofJournal of Cerebral Blood Flow & Metabolism-
dc.titleSelective astrocytic endothelin-1 overexpression contributes to dementia associated with ischemic stroke by exaggerating astrocyte-derived amyloid secretion-
dc.typeArticle-
dc.identifier.emailYeung, PKK: ykkp@hkucc.hku.hk-
dc.identifier.emailLo, ACY: amylo@hku.hk-
dc.identifier.emailWu, EX: ewu@eee.hku.hk-
dc.identifier.emailChung, SK: skchung@hkucc.hku.hk-
dc.identifier.authorityLo, ACY=rp00425-
dc.identifier.authorityWu, EX=rp00193-
dc.identifier.authorityChung, SK=rp00381-
dc.identifier.doi10.1038/jcbfm.2015.109-
dc.identifier.hkuros254461-

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