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Article: Rapid regulation of adrenomedullin in metabolically compromised vascular smooth muscle cells

TitleRapid regulation of adrenomedullin in metabolically compromised vascular smooth muscle cells
Authors
Keywords2-Deoxyglucose
Adrenomedullin
ATP
Glycolysis
Vascular smooth muscle
Vasodilator
Issue Date1999
PublisherLippincott Williams & Wilkins, Ltd. The Journal's web site is located at http://www.jhypertension.com/
Citation
Journal Of Hypertension, 1999, v. 17 n. 3, p. 373-379 How to Cite?
AbstractObjective. The prepro-adrenomedullin gene encodes the biologically active peptide adrenomedullin, which acts as a potent vasodilator as well as a modulator of vascular smooth muscle cell growth. We investigated the question of whether adrenomedullin is regulated in response to metabolic perturbations in vascular smooth muscle. Materials and methods. Acute inhibition of glycolysis, leading to partial depletion of cellular ATP, was produced in cultured rat aortic vascular smooth muscle cells by replacing glucose with 2-deoxyglucose. Solution hybridization/RNase protection analysis was used to quantitate changes in expression of the prepro-adrenomedullin messenger RNA and a specific radioimmunoassay was used to assess levels of secreted adrenomedullin. Results. Acute incubation of rat aortic vascular smooth muscle cells with 2-deoxyglucose caused a rapid and sustained induction of low basal levels of adrenomedullin messenger RNA, which reached twice the control levels by 1 h and four times control levels by 6 h. The induction of adrenomedullin messenger RNA expression was dependent upon de-novo gene transcription and was reversed by the re-introduction of glucose. Despite the sustained increase in adrenomedullin messenger RNA, secretion of immunoreactive-adrenomedullin from vascular smooth muscle cells was reduced by as much as 75% and paralleled the inhibition of radiolabeled amino acid incorporation into protein during glycolytic inhibition; both parameters recovered towards control levels following re-introduction of glucose. Conclusions. The rapid and reversible activation of the adrenomedullin gene and inhibition of adrenomedullin peptide release in response to metabolic inhibition suggest that adrenomedullin represents a novel localized mechanism that may modulate regional blood flow and vascular smooth muscle cell proliferation in response to perturbations of normal metabolism.
Persistent Identifierhttp://hdl.handle.net/10722/81130
ISSN
2015 Impact Factor: 5.062
2015 SCImago Journal Rankings: 2.193
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorAutelitano, DJen_HK
dc.contributor.authorTang, Fen_HK
dc.contributor.authorLittle, PJen_HK
dc.date.accessioned2010-09-06T08:14:10Z-
dc.date.available2010-09-06T08:14:10Z-
dc.date.issued1999en_HK
dc.identifier.citationJournal Of Hypertension, 1999, v. 17 n. 3, p. 373-379en_HK
dc.identifier.issn0263-6352en_HK
dc.identifier.urihttp://hdl.handle.net/10722/81130-
dc.description.abstractObjective. The prepro-adrenomedullin gene encodes the biologically active peptide adrenomedullin, which acts as a potent vasodilator as well as a modulator of vascular smooth muscle cell growth. We investigated the question of whether adrenomedullin is regulated in response to metabolic perturbations in vascular smooth muscle. Materials and methods. Acute inhibition of glycolysis, leading to partial depletion of cellular ATP, was produced in cultured rat aortic vascular smooth muscle cells by replacing glucose with 2-deoxyglucose. Solution hybridization/RNase protection analysis was used to quantitate changes in expression of the prepro-adrenomedullin messenger RNA and a specific radioimmunoassay was used to assess levels of secreted adrenomedullin. Results. Acute incubation of rat aortic vascular smooth muscle cells with 2-deoxyglucose caused a rapid and sustained induction of low basal levels of adrenomedullin messenger RNA, which reached twice the control levels by 1 h and four times control levels by 6 h. The induction of adrenomedullin messenger RNA expression was dependent upon de-novo gene transcription and was reversed by the re-introduction of glucose. Despite the sustained increase in adrenomedullin messenger RNA, secretion of immunoreactive-adrenomedullin from vascular smooth muscle cells was reduced by as much as 75% and paralleled the inhibition of radiolabeled amino acid incorporation into protein during glycolytic inhibition; both parameters recovered towards control levels following re-introduction of glucose. Conclusions. The rapid and reversible activation of the adrenomedullin gene and inhibition of adrenomedullin peptide release in response to metabolic inhibition suggest that adrenomedullin represents a novel localized mechanism that may modulate regional blood flow and vascular smooth muscle cell proliferation in response to perturbations of normal metabolism.en_HK
dc.languageengen_HK
dc.publisherLippincott Williams & Wilkins, Ltd. The Journal's web site is located at http://www.jhypertension.com/en_HK
dc.relation.ispartofJournal of Hypertensionen_HK
dc.rightsJournal of Hypertension. Copyright © Lippincott Williams & Wilkins, Ltd.en_HK
dc.subject2-Deoxyglucoseen_HK
dc.subjectAdrenomedullinen_HK
dc.subjectATPen_HK
dc.subjectGlycolysisen_HK
dc.subjectVascular smooth muscleen_HK
dc.subjectVasodilatoren_HK
dc.titleRapid regulation of adrenomedullin in metabolically compromised vascular smooth muscle cellsen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0263-6352&volume=17&spage=373&epage=379&date=1999&atitle=Rapid+regulation+of+adrenomedullin+in+metabolically+compromised+vascular+smooth+muscle+cellsen_HK
dc.identifier.emailTang, F: ftang@hkucc.hku.hken_HK
dc.identifier.authorityTang, F=rp00327en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1097/00004872-199917030-00010en_HK
dc.identifier.pmid10100075-
dc.identifier.scopuseid_2-s2.0-0033016188en_HK
dc.identifier.hkuros44129en_HK
dc.identifier.hkuros53236-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033016188&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume17en_HK
dc.identifier.issue3en_HK
dc.identifier.spage373en_HK
dc.identifier.epage379en_HK
dc.identifier.isiWOS:000079235800010-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridAutelitano, DJ=7003803451en_HK
dc.identifier.scopusauthoridTang, F=7201979770en_HK
dc.identifier.scopusauthoridLittle, PJ=7201985910en_HK

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