File Download

There are no files associated with this item.

  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Reversal of diabetes-evoked changes in mitochondrial protein expression of cardiac left ventricle by treatment with a copper (II)-selective chelator

TitleReversal of diabetes-evoked changes in mitochondrial protein expression of cardiac left ventricle by treatment with a copper (II)-selective chelator
Authors
KeywordsDiabetic cardiomyopathy
Diabetic complications
Diastolic heart failure
Electron transport chain
Left ventricular hypertrophy
Issue Date2007
PublisherWiley - V C H Verlag GmbH & Co KGaA.
Citation
Proteomics - Clinical Applications, 2007, v. 1 n. 4, p. 387-399 How to Cite?
AbstractCardiac disease is the commonest cause of death amongst diabetic patients. Diabetic cardiomyopathy, which has a poor prognosis, is characterized by left ventricular hypertrophy and impaired cardiac function and mitochondrial damage is said to contribute to its development. We recently showed that treatment with the CuII-selective chelator, triethylenetetramine (TETA), improved cardiac structure, and function in diabetic subjects without modifying hyperglycemia. Thus, TETA has potential utility for the treatment of heart disease. To further understand the molecular mechanism by which it causes these effects, we have conducted the first study of the effect of oral TETA on protein abundance in the cardiac left ventricle of rats with severe streptozotocin-induced diabetes. Proteomic methods showed that of 211 proteins changed in diabetes, 33 recovered after treatment. Through MS, 16 proteins were identified which may constitute major targets of drug action. Remarkably, most of these were mitochondrial proteins with Toles in energy metabolism. In addition to components of the mitochondrial respiratory chain and enzymes involved in fatty add oxidation, TETA treatment normalized both myocardial expression and enzymatic activity of carnitine palmitoyltransferase 2. These findings indicate that mitochondria constitute major targets in the mechanism by which TETA restores cardiac structure and function in diabetes. © 2007 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.
Persistent Identifierhttp://hdl.handle.net/10722/77675
ISSN
2015 Impact Factor: 2.959
2015 SCImago Journal Rankings: 1.117
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorJüllig, Men_HK
dc.contributor.authorChen, Xen_HK
dc.contributor.authorHickey, AJen_HK
dc.contributor.authorCrossman, DJen_HK
dc.contributor.authorXu, Aen_HK
dc.contributor.authorWang, Yen_HK
dc.contributor.authorGreenwood, DRen_HK
dc.contributor.authorChoong, YSen_HK
dc.contributor.authorSchönberger, SJen_HK
dc.contributor.authorMiddleditch, MJen_HK
dc.contributor.authorPhillips, ARJen_HK
dc.contributor.authorCooper, GJSen_HK
dc.date.accessioned2010-09-06T07:34:29Z-
dc.date.available2010-09-06T07:34:29Z-
dc.date.issued2007en_HK
dc.identifier.citationProteomics - Clinical Applications, 2007, v. 1 n. 4, p. 387-399en_HK
dc.identifier.issn1862-8346en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77675-
dc.description.abstractCardiac disease is the commonest cause of death amongst diabetic patients. Diabetic cardiomyopathy, which has a poor prognosis, is characterized by left ventricular hypertrophy and impaired cardiac function and mitochondrial damage is said to contribute to its development. We recently showed that treatment with the CuII-selective chelator, triethylenetetramine (TETA), improved cardiac structure, and function in diabetic subjects without modifying hyperglycemia. Thus, TETA has potential utility for the treatment of heart disease. To further understand the molecular mechanism by which it causes these effects, we have conducted the first study of the effect of oral TETA on protein abundance in the cardiac left ventricle of rats with severe streptozotocin-induced diabetes. Proteomic methods showed that of 211 proteins changed in diabetes, 33 recovered after treatment. Through MS, 16 proteins were identified which may constitute major targets of drug action. Remarkably, most of these were mitochondrial proteins with Toles in energy metabolism. In addition to components of the mitochondrial respiratory chain and enzymes involved in fatty add oxidation, TETA treatment normalized both myocardial expression and enzymatic activity of carnitine palmitoyltransferase 2. These findings indicate that mitochondria constitute major targets in the mechanism by which TETA restores cardiac structure and function in diabetes. © 2007 Wiley-VCH Verlag GmbH & Co. KGaA, Weinheim.en_HK
dc.languageengen_HK
dc.publisherWiley - V C H Verlag GmbH & Co KGaA.en_HK
dc.relation.ispartofProteomics - Clinical Applicationsen_HK
dc.subjectDiabetic cardiomyopathyen_HK
dc.subjectDiabetic complicationsen_HK
dc.subjectDiastolic heart failureen_HK
dc.subjectElectron transport chainen_HK
dc.subjectLeft ventricular hypertrophyen_HK
dc.titleReversal of diabetes-evoked changes in mitochondrial protein expression of cardiac left ventricle by treatment with a copper (II)-selective chelatoren_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1862-8346&volume=1&spage=387&epage=99&date=2007&atitle=Reversal+of+diabetes-evoked+changes+in+mitochondrial+protein+expression+of+cardiac+left+ventricle+by+treatment+with+a+copper(II)-selective+chelatoren_HK
dc.identifier.emailXu, A: amxu@hkucc.hku.hken_HK
dc.identifier.emailWang, Y: yuwanghk@hku.hken_HK
dc.identifier.authorityXu, A=rp00485en_HK
dc.identifier.authorityWang, Y=rp00239en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1002/prca.200600770en_HK
dc.identifier.scopuseid_2-s2.0-34748841342en_HK
dc.identifier.hkuros140658en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34748841342&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1en_HK
dc.identifier.issue4en_HK
dc.identifier.spage387en_HK
dc.identifier.epage399en_HK
dc.identifier.isiWOS:000246615600004-
dc.publisher.placeGermanyen_HK
dc.identifier.scopusauthoridJüllig, M=6507058081en_HK
dc.identifier.scopusauthoridChen, X=15064988500en_HK
dc.identifier.scopusauthoridHickey, AJ=7006559720en_HK
dc.identifier.scopusauthoridCrossman, DJ=7005689853en_HK
dc.identifier.scopusauthoridXu, A=7202655409en_HK
dc.identifier.scopusauthoridWang, Y=34973733700en_HK
dc.identifier.scopusauthoridGreenwood, DR=35233357400en_HK
dc.identifier.scopusauthoridChoong, YS=36797592700en_HK
dc.identifier.scopusauthoridSchönberger, SJ=26324370000en_HK
dc.identifier.scopusauthoridMiddleditch, MJ=23397792300en_HK
dc.identifier.scopusauthoridPhillips, ARJ=25931065800en_HK
dc.identifier.scopusauthoridCooper, GJS=7402355946en_HK

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats