| Calcineurin activates cytoglobin transcription in hypoxic myocytes. | |
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MedLine Citation:
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PMID: 19203999 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Cardiac hypertrophy develops in response to a variety of cardiovascular stresses and results in activation of numerous signaling cascades and proteins. In the present study, we demonstrate that cytoglobin is a stress-responsive hemoprotein in the hypoxia-induced hypertrophic myocardium and it is transcriptionally regulated by calcineurin-dependent transcription factors. The cytoglobin transcript level is abundantly expressed in the adult heart and in response to hypoxia cytoglobin expression is markedly up-regulated within the hypoxia-induced hypertrophic heart. To define the molecular mechanism resulting in the induction of cytoglobin, we undertook a transcriptional analysis of the 5' upstream regulatory region of the cytoglobin gene. Evolutionarily conserved binding elements for transcription factors HIF-1, AP-1, and NFAT are located within the upstream region of the cytoglobin gene. Transcriptional assays demonstrated that calcineurin activity modulates cytoglobin transcription. Increased calcineurin activity enhances the ability of NFAT and AP-1 to bind to the putative cytoglobin promoter, especially under hypoxic conditions. In addition, inhibition of calcineurin, NFAT, and/or AP-1 activities decreases endogenous cytoglobin transcript and protein levels. Thus, the regulation of cytoglobin transcription by calcineurin-dependent transcription factors suggests that cytoglobin may have a functional role in calcium-dependent events accompanying cardiac remodeling. |
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Authors:
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Sarvjeet Singh; Shilpa M Manda; Devanjan Sikder; Michael J Birrer; Beverly A Rothermel; Daniel J Garry; Pradeep P A Mammen |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2009-02-09 |
Journal Detail:
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Title: The Journal of biological chemistry Volume: 284 ISSN: 0021-9258 ISO Abbreviation: J. Biol. Chem. Publication Date: 2009 Apr |
Date Detail:
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Created Date: 2009-04-13 Completed Date: 2009-06-18 Revised Date: 2010-09-23 |
Medline Journal Info:
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Nlm Unique ID: 2985121R Medline TA: J Biol Chem Country: United States |
Other Details:
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Languages: eng Pagination: 10409-21 Citation Subset: IM |
Affiliation:
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Departments of Internal Medicine and Molecular Biology, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anoxia* / metabolism Base Sequence Calcineurin / genetics, metabolism* Cell Line Globins / genetics, metabolism* Humans Hypertrophy, Left Ventricular / metabolism JNK Mitogen-Activated Protein Kinases / genetics, metabolism Male Mice Mice, Inbred C57BL Mice, Transgenic Mutagenesis, Site-Directed Myocytes, Cardiac / cytology, physiology* Promoter Regions, Genetic / genetics Proto-Oncogene Proteins c-fos / genetics, metabolism Rats Response Elements / genetics Sequence Alignment Transcriptional Activation* |
| Grant Support | |
ID/Acronym/Agency:
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HL-076440/HL/NHLBI NIH HHS; HL-63788/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Proto-Oncogene Proteins c-fos; 0/cytoglobin; 9004-22-2/Globins; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases; EC 3.1.3.16/Calcineurin |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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