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Article: Endothelin-1 protects astrocytes from hypoxic/ischemic injury

TitleEndothelin-1 protects astrocytes from hypoxic/ischemic injury
Authors
KeywordsCell survival
Endothelin receptors
Endothelin-3
ET-1-deficient mice
Lactate dehydrogenase
Issue Date2001
PublisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/
Citation
FASEB Journal, 2001, v. 15 n. 3, p. 618-626 How to Cite?
AbstractUnder pathological conditions such as ischemia (I), subarachnoid hemorrhage, and Alzheimer's disease, astrocytes show a large increase in endothelin (ET) -like immunoreactivity. However, it is not clear whether ET is protective or destructive to these cells during brain injury. Using astrocytes from ET-1-deficient mice, we determined the effect of ET-1 on these cells under normal, hypoxic (H), and hypoxic/ischemic (H/I) conditions. Under normal culture conditions, astrocytes from wild-type and ET-1-deficient mice showed no difference in their morphology and cell proliferation rates. ET-3 and ETA receptor mRNAs were up-regulated whereas ETB receptor mRNA was down-regulated in ET-1-deficient astrocytes, suggesting that ET-1 and ET-3 may complement each other's functions and that the expressions of these endothelins and their receptors are regulated by a complex feedback mechanism. Under H and H/I conditions, ET-1 peptide and mRNA were up-regulated in wild-type astrocytes, and the astrocytes without ET-1 died faster than the wild-type astrocytes, as indicated by greater efflux of lactate dehydrogenase. The present study suggests that astrocytes without ET-1 are more vulnerable to H and H/I injuries and that the up-regulation of astrocytic ET-1 is essential for the survival of astrocytes.
Persistent Identifierhttp://hdl.handle.net/10722/88024
ISSN
2015 Impact Factor: 5.299
2015 SCImago Journal Rankings: 2.775
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorHo, MCYen_HK
dc.contributor.authorLo, ACYen_HK
dc.contributor.authorKurihara, Hen_HK
dc.contributor.authorYu, ACHen_HK
dc.contributor.authorChung, SSMen_HK
dc.contributor.authorChung, SKen_HK
dc.date.accessioned2010-09-06T09:37:39Z-
dc.date.available2010-09-06T09:37:39Z-
dc.date.issued2001en_HK
dc.identifier.citationFASEB Journal, 2001, v. 15 n. 3, p. 618-626en_HK
dc.identifier.issn0892-6638en_HK
dc.identifier.urihttp://hdl.handle.net/10722/88024-
dc.description.abstractUnder pathological conditions such as ischemia (I), subarachnoid hemorrhage, and Alzheimer's disease, astrocytes show a large increase in endothelin (ET) -like immunoreactivity. However, it is not clear whether ET is protective or destructive to these cells during brain injury. Using astrocytes from ET-1-deficient mice, we determined the effect of ET-1 on these cells under normal, hypoxic (H), and hypoxic/ischemic (H/I) conditions. Under normal culture conditions, astrocytes from wild-type and ET-1-deficient mice showed no difference in their morphology and cell proliferation rates. ET-3 and ETA receptor mRNAs were up-regulated whereas ETB receptor mRNA was down-regulated in ET-1-deficient astrocytes, suggesting that ET-1 and ET-3 may complement each other's functions and that the expressions of these endothelins and their receptors are regulated by a complex feedback mechanism. Under H and H/I conditions, ET-1 peptide and mRNA were up-regulated in wild-type astrocytes, and the astrocytes without ET-1 died faster than the wild-type astrocytes, as indicated by greater efflux of lactate dehydrogenase. The present study suggests that astrocytes without ET-1 are more vulnerable to H and H/I injuries and that the up-regulation of astrocytic ET-1 is essential for the survival of astrocytes.en_HK
dc.languageengen_HK
dc.publisherFederation of American Societies for Experimental Biology. The Journal's web site is located at http://www.fasebj.org/en_HK
dc.relation.ispartofFASEB Journalen_HK
dc.subjectCell survivalen_HK
dc.subjectEndothelin receptorsen_HK
dc.subjectEndothelin-3en_HK
dc.subjectET-1-deficient miceen_HK
dc.subjectLactate dehydrogenaseen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAstrocytes - drug effects - physiologyen_HK
dc.subject.meshBlotting, Westernen_HK
dc.subject.meshBrain Chemistryen_HK
dc.subject.meshCell Divisionen_HK
dc.subject.meshCell Hypoxiaen_HK
dc.subject.meshCell Sizeen_HK
dc.subject.meshCells, Cultureden_HK
dc.subject.meshCulture Media, Serum-Freeen_HK
dc.subject.meshEndothelin-1 - genetics - metabolism - pharmacologyen_HK
dc.subject.meshEndothelin-3 - genetics - metabolismen_HK
dc.subject.meshFemaleen_HK
dc.subject.meshGene Expression Regulationen_HK
dc.subject.meshGlial Fibrillary Acidic Protein - genetics - metabolismen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshL-Lactate Dehydrogenase - secretionen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshNeuroprotective Agentsen_HK
dc.subject.meshRNA, Messenger - metabolismen_HK
dc.subject.meshReceptors, Endothelin - genetics - metabolismen_HK
dc.subject.meshReverse Transcriptase Polymerase Chain Reactionen_HK
dc.titleEndothelin-1 protects astrocytes from hypoxic/ischemic injuryen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0892-6638&volume=15&spage=618&epage=626&date=2001&atitle=Endothelin-1+protects+astrocytes+from+hypoxic/ischemic+injuryen_HK
dc.identifier.emailLo, ACY: amylo@hkucc.hku.hken_HK
dc.identifier.emailChung, SSM: smchung@hkucc.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.authorityLo, ACY=rp00425en_HK
dc.identifier.authorityChung, SSM=rp00376en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1096/fj.99-1022comen_HK
dc.identifier.pmid11259380-
dc.identifier.scopuseid_2-s2.0-0035085831en_HK
dc.identifier.hkuros60023en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0035085831&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume15en_HK
dc.identifier.issue3en_HK
dc.identifier.spage618en_HK
dc.identifier.epage626en_HK
dc.identifier.isiWOS:000167419500019-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridHo, MCY=7403080620en_HK
dc.identifier.scopusauthoridLo, ACY=7102780640en_HK
dc.identifier.scopusauthoridKurihara, H=35398101800en_HK
dc.identifier.scopusauthoridYu, ACH=7401478731en_HK
dc.identifier.scopusauthoridChung, SSM=14120761600en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK

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