Document Detail


Folic acid mitigated cardiac dysfunction by normalizing the levels of tissue inhibitor of metalloproteinase and homocysteine-metabolizing enzymes postmyocardial infarction in mice.
MedLine Citation:
PMID:  20802128     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Natia Qipshidze; Neetu Tyagi; Utpal Sen; Srikanth Givvimani; Naira Metreveli; David Lominadze; Suresh C Tyagi
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-08-27
Journal Detail:
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:
Created Date:  2010-11-01     Completed Date:  2010-11-29     Revised Date:  2013-05-28    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H1484-93     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, School of Medicine, University of Louisville, Louisville, Kentucky 40202, USA.
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MeSH Terms
Descriptor/Qualifier:
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:
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:
0/Hematinics; 0/Tissue Inhibitor of Metalloproteinases; 454-28-4/Homocysteine; 59-30-3/Folic Acid; EC 3.4.24.-/Matrix Metalloproteinases
Comments/Corrections

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