| Folic acid mitigated cardiac dysfunction by normalizing the levels of tissue inhibitor of metalloproteinase and homocysteine-metabolizing enzymes postmyocardial infarction in mice. | |
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MedLine Citation:
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PMID: 20802128 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Myocardial infarction (MI) results in significant metabolic derangement, causing accumulation of metabolic by product, such as homocysteine (Hcy). Hcy is a nonprotein amino acid generated during nucleic acid methylation and demethylation of methionine. Folic acid (FA) decreases Hcy levels by remethylating the Hcy to methionine, by 5-methylene tetrahydrofolate reductase (5-MTHFR). Although clinical trials were inconclusive regarding the role of Hcy in MI, in animal models, the levels of 5-MTHFR were decreased, and FA mitigated the MI injury. We hypothesized that FA mitigated MI-induced injury, in part, by mitigating cardiac remodeling during chronic heart failure. Thus, MI was induced in 12-wk-old male C57BL/J mice by ligating the left anterior descending artery, and FA (0.03 g/l in drinking water) was administered for 4 wk after the surgery. Cardiac function was assessed by echocardiography and by a Millar pressure-volume catheter. The levels of Hcy-metabolizing enzymes, cystathionine β-synthase (CBS), cystathionine γ-lyase (CSE), and 5-MTHFR, were estimated by Western blot analyses. The results suggest that FA administered post-MI significantly improved cardiac ejection fraction and induced tissue inhibitor of metalloproteinase, CBS, CSE, and 5-MTHFR. We showed that FA supplementation resulted in significant improvement of myocardial function after MI. The study eluted the importance of homocysteine (Hcy) metabolism and FA supplementation in cardiovascular disease. |
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Authors:
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Natia Qipshidze; Neetu Tyagi; Utpal Sen; Srikanth Givvimani; Naira Metreveli; David Lominadze; Suresh C Tyagi |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2010-08-27 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 299 ISSN: 1522-1539 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2010 Nov |
Date Detail:
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Created Date: 2010-11-01 Completed Date: 2010-11-29 Revised Date: 2011-11-01 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1484-93 Citation Subset: IM |
Affiliation:
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Department of Physiology and Biophysics, School of Medicine, University of Louisville, Louisville, Kentucky 40202, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Dietary Supplements Folic Acid / administration & dosage, pharmacology*, therapeutic use Heart / drug effects*, physiopathology Hematinics / administration & dosage, pharmacology*, therapeutic use Homocysteine / metabolism* Male Matrix Metalloproteinases / metabolism* Mice Mice, Inbred C57BL Models, Animal Myocardial Infarction / drug therapy, metabolism* Myocytes, Cardiac / drug effects, physiology Neovascularization, Physiologic / drug effects, physiology Tissue Inhibitor of Metalloproteinases / metabolism* Treatment Outcome Ventricular Function, Left / drug effects, physiology |
| Grant Support | |
ID/Acronym/Agency:
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HL-71010/HL/NHLBI NIH HHS; HL-74185/HL/NHLBI NIH HHS; HL-80394/HL/NHLBI NIH HHS; HL-88012/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Hematinics; 0/Tissue Inhibitor of Metalloproteinases; 454-28-4/Homocysteine; 59-30-3/Folic Acid; EC 3.4.24.-/Matrix Metalloproteinases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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