| Activated NHE1 is required to induce early cardiac hypertrophy in mice. | |
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MedLine Citation:
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PMID: 21359875 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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The Na(+)/H(+) exchanger isoform 1 (NHE1) has been implicated as being causal in cardiac hypertrophy and the protein level and activity are elevated in the diseased myocardium. However, it is unclear whether mere elevation of the protein is sufficient for cardiac pathology, or whether activation of the protein is required. In this study, we examined the comparative effects of elevation of wild type and activated NHE1. Two mouse transgenic models that expressed either a wild type NHE1 protein or an activated NHE1 protein were characterized. Expression of activated NHE1 caused significant increases in heart weight to body weight, apoptosis, cross-sectional area, interstitial fibrosis and decreased cardiac performance. Expression of wild type NHE1 caused a much milder pathology. When we examined 2 or 10-week-old mouse hearts, there was neither elevation of calcineurin levels nor increased phosphorylation of ERK or p38 in either NHE1 transgenic mouse line. Expression of activated NHE1 in intact mice caused an increased sensitivity to phenylephrine-induced hypertrophy. Our results show that expression of activated NHE1 promotes cardiac hypertrophy to a much greater degree than elevated levels of wild type NHE1 alone. In addition, expression of activated NHE1 promotes greater sensitivity to neurohormonal stimulation. The results suggest that activation of NHE1 is a key component that accentuates NHE1-induced myocardial pathology. |
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Authors:
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Fatima Mraiche; Tatsujiro Oka; Xiaohong T Gan; Morris Karmazyn; Larry Fliegel |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-2-27 |
Journal Detail:
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Title: Basic research in cardiology Volume: - ISSN: 1435-1803 ISO Abbreviation: - Publication Date: 2011 Feb |
Date Detail:
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Created Date: 2011-3-1 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0360342 Medline TA: Basic Res Cardiol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Department of Biochemistry, University of Alberta, Edmonton, AB T6G 2H7, Canada. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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