Document Detail


Short-term magnesium deficiency upregulates ceramide synthase in cardiovascular tissues and cells: cross-talk among cytokines, Mg2+, NF-κB, and de novo ceramide.
MedLine Citation:
PMID:  21984552     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The present study tested the hypotheses that 1) short-term dietary deficiency (MgD) of magnesium (21 days) would result in the upregulation of ceramide synthase (CS) in left ventricular (LV), right ventricular, atrial, and aortic smooth muscle, as well as induce a synthesis/release of select cytokines and chemokines into the LV and aortic smooth muscle and serum; 2) exposure of primary cultured vascular smooth muscle cells (VSMCs) to low extracellular Mg concentration would lead to the synthesis/release of select cytokines/chemokines, activation of N-SMase, and the de novo synthesis of ceramide; and 3) inhibition of CS by fumonisin B1 (FB1) or inhibition of neutral sphingomyelinase (N-SMase) by scyphostatin (SCY) in VSMCs exposed to low Mg would result in reductions in the levels of the cytokines/chemokines and lowered levels of ceramide concomitant with inhibition of NF-κB activation. The data indicated that short-term MgD (10% normal dietary intake) resulted in the upregulation of CS in ventricular, atrial, and aortic smooth muscles coupled to the synthesis/release of 12 different cytokines/chemokines, as well as activation of NF-κB in the LV and aortic smooth muscle and sera; even very low levels of water-borne Mg (e.g., 15 mg·l(-1)·day(-1)) either prevented or ameliorated the upregulation and synthesis of the cytokines/chemokines. Our experiments also showed that VSMCs exposed to low extracellular Mg resulted in the synthesis of 5 different cytokines and chemokines concomitant with synthesis/release of ceramide. However, inhibition of the synthesis and release of ceramide by either FB1 or SCY attenuated, markedly , the generation of ceramide, release of the cytokines/chemokines, and activation of NF-κB (as measured by activated p65 and cRel).
Authors:
Burton M Altura; Nilank C Shah; Gatha Shah; Aimin Zhang; Wenyan Li; Tao Zheng; Jose Luis Perez-Albela; Bella T Altura
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2011-10-07
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  302     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2012 Jan 
Date Detail:
Created Date:  2011-12-27     Completed Date:  2012-02-14     Revised Date:  2012-05-23    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H319-32     Citation Subset:  IM    
Affiliation:
Department of Physiology and Pharmacology, State University of New York Downstate Medical Center, Brooklyn, 11203, USA. baltura@downstate.edu
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MeSH Terms
Descriptor/Qualifier:
Amides / pharmacology
Animals
Aorta / metabolism
Cells, Cultured
Ceramides / metabolism*
Cytokines / metabolism*
Diet
Disease Models, Animal
Drinking
Eating
Enzyme Inhibitors / pharmacology
Female
Fumonisins / pharmacology
Heart Atria / enzymology
Heart Ventricles / enzymology
Magnesium / administration & dosage,  metabolism*
Magnesium Deficiency / enzymology*,  prevention & control
Male
Muscle, Smooth, Vascular / drug effects,  enzymology*
Myocytes, Cardiac / drug effects,  enzymology*
NF-kappa B / metabolism*
Oxidoreductases / antagonists & inhibitors,  metabolism*
Proto-Oncogene Proteins c-rel / metabolism
Pyrones / pharmacology
Rats
Regression Analysis
Signal Transduction
Sphingomyelin Phosphodiesterase / antagonists & inhibitors,  metabolism
Time Factors
Transcription Factor RelA / metabolism
Up-Regulation
Chemical
Reg. No./Substance:
0/Amides; 0/Ceramides; 0/Cytokines; 0/Enzyme Inhibitors; 0/Fumonisins; 0/NF-kappa B; 0/Proto-Oncogene Proteins c-rel; 0/Pyrones; 0/Rela protein, rat; 0/Transcription Factor RelA; 0/scyphostatin; 116355-83-0/fumonisin B1; 7439-95-4/Magnesium; EC 1.-/Oxidoreductases; EC 1.3.1.-/dihydroceramide desaturase; EC 3.1.4.12/Sphingomyelin Phosphodiesterase

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