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dc.contributor.author Sentex, E
dc.contributor.author Wang, X
dc.contributor.author Liu, XL
dc.contributor.author Lukas, A
dc.contributor.author Dhalla, NS
dc.date.accessioned 2007-10-05T15:45:08Z
dc.date.available 2007-10-05T15:45:08Z
dc.date.issued 2006-02-28
dc.identifier.citation 0008-4212; CAN J PHYSIOL PHARMACOL, FEB 2006, vol. 84, no. 2, p.227 to 238. en
dc.identifier.uri http://hdl.handle.net/1993/2894
dc.description.abstract The present study determined whether changes in the activity and isoforms of protein kinase C (PKC) are associated with cardiac hypertrophy and heart failure owing to volume overload induced by aortocaval shunt (AVS) in rats. A significant increase in Ca2+-dependent and Ca2+-independent PKC activities in the homogenate and particulate fractions, unlike the cystolic fraction, of the hypertrophied left ventricle (LV) were evident at 2 and 4 weeks after inducing the AVS. This increase coincided with increases in PKC-alpha and PKC-zeta contents at 2 week and increases in PKC-alpha, PKC-beta(1), PKC-beta(2), and PKC-zeta contents at 4 weeks in the hypertrophied LV. By 8 and 16 weeks of AVS, PKC activity and content were unchanged in the failing LV. On the other hand, no increase in the PKC activity or isoform content in the hypertrophied right ventricle (RV) was observed during the 16 weeks of AVS. The content of G alpha q was increased in the LV at 2 weeks but then decreased at 16 weeks, whereas G alpha q content was increased in RV at 2 and 4 weeks. Our data suggest that an increase in PKC isoform content neither plays an important role during the development of cardiac hypertrophy nor participates in the phase leading to heart failure owing to volume overload. en
dc.format.extent 658597 bytes
dc.format.mimetype application/pdf
dc.language.iso en_US
dc.rights No part of the NRC Research Press electronic journals may be reproduced, stored, or transmitted in any form or by any means, without the written permission of the publisher, except as stated below. Under the Canadian Copyright Act, individuals may download or print single copies of articles for personal research or study. Any person may reproduce short excerpts from articles in the journals for any purpose that respects the moral rights of authors, provided that the source is fully acknowledged. As a courtesy, the consent of authors of such material should be obtained directly from the author. Authorization to reproduce items for other than personal research or study, as stated above, may be obtained via Access © upon payment of the copyright fee of $10.00 per copy. NRC Research Press also extends certain additional rights to authors. The above rights do not extend to copying or reproduction for general distribution, for advertising or promotional purposes, for creating new collective works, or for resale. For such copying or reproduction, arrangements must be made with NRC Research Press. en
dc.subject protein kinase C en
dc.subject volume overload en
dc.subject cardiac hypertrophy en
dc.subject heart failure en
dc.subject LEFT-VENTRICULAR HYPERTROPHY en
dc.subject MYOCARDIAL-INFARCTION en
dc.subject RAT en
dc.subject PKC en
dc.subject ACTIVATION en
dc.subject ISOZYMES en
dc.subject EPSILON en
dc.subject BETA en
dc.subject TRANSLOCATION en
dc.subject MYOCYTES en
dc.title Expression of protein kinase C isoforms in cardiac hypertrophy and heart failure due to volume overload en
dc.status Peer reviewed en
dc.identifier.doi http://dx.doi.org/10.1139/y05-120


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