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Myocardial infarction differentially alters sphingolipid levels in plasma, erythrocytes and platelets of the rat

Three bioactive sphingolipids, namely sphingosine-1-phosphate (S1P), ceramide (CER) and sphingosine (SPH) were shown to be involved in ischemia/reperfusion injury of the heart. S1P is a powerful cardioprotectant, CER activates apoptosis and SPH in a low dose is cardioprotective whereas in a high dos...

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Autores principales: Knapp, Małgorzata, Żendzian-Piotrowska, Małgorzata, Błachnio-Zabielska, Agnieszka, Zabielski, Piotr, Kurek, Krzysztof, Górski, Jan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer-Verlag 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505520/
https://www.ncbi.nlm.nih.gov/pubmed/22961594
http://dx.doi.org/10.1007/s00395-012-0294-0
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author Knapp, Małgorzata
Żendzian-Piotrowska, Małgorzata
Błachnio-Zabielska, Agnieszka
Zabielski, Piotr
Kurek, Krzysztof
Górski, Jan
author_facet Knapp, Małgorzata
Żendzian-Piotrowska, Małgorzata
Błachnio-Zabielska, Agnieszka
Zabielski, Piotr
Kurek, Krzysztof
Górski, Jan
author_sort Knapp, Małgorzata
collection PubMed
description Three bioactive sphingolipids, namely sphingosine-1-phosphate (S1P), ceramide (CER) and sphingosine (SPH) were shown to be involved in ischemia/reperfusion injury of the heart. S1P is a powerful cardioprotectant, CER activates apoptosis and SPH in a low dose is cardioprotective whereas in a high dose is cardiotoxic. The aim of the present study was to examine effects of experimental myocardial infarction on the level of selected sphingolipids in plasma, erythrocytes and platelets in the rat. Myocardial infarction was produced in male Wistar rats by ligation of the left coronary artery. Blood was taken from the abdominal aorta at 1, 6 and 24 h after the ligation. Plasma, erythrocytes and platelets were isolated and S1P, dihydrosphingosine-1-phosphate (DHS1P), SPH, dihydrosphingosine (DHS) and CER were quantified by means of an Agilent 6460 triple quadrupole mass spectrometer using positive ion electrospray ionization source with multiple reaction monitoring. The infarction reduced the plasma level of S1P, DHS1P, SPH and DHS but increased the level of total CER. In erythrocytes, there was a sharp elevation in the level of SPH and DHS early after the infarction and a reduction after 24 h whereas the level of S1P, DHS1P and total CER gradually increased. In platelets, the level of each of the examined compounds profoundly decreased 1 and 6 h after the infarction and partially normalized in 24 h. The results obtained clearly show that experimental heart infarction in rats produces deep changes in metabolism of sphingolipids in the plasma, platelets and erythrocytes.
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spelling pubmed-35055202012-11-28 Myocardial infarction differentially alters sphingolipid levels in plasma, erythrocytes and platelets of the rat Knapp, Małgorzata Żendzian-Piotrowska, Małgorzata Błachnio-Zabielska, Agnieszka Zabielski, Piotr Kurek, Krzysztof Górski, Jan Basic Res Cardiol Original Contribution Three bioactive sphingolipids, namely sphingosine-1-phosphate (S1P), ceramide (CER) and sphingosine (SPH) were shown to be involved in ischemia/reperfusion injury of the heart. S1P is a powerful cardioprotectant, CER activates apoptosis and SPH in a low dose is cardioprotective whereas in a high dose is cardiotoxic. The aim of the present study was to examine effects of experimental myocardial infarction on the level of selected sphingolipids in plasma, erythrocytes and platelets in the rat. Myocardial infarction was produced in male Wistar rats by ligation of the left coronary artery. Blood was taken from the abdominal aorta at 1, 6 and 24 h after the ligation. Plasma, erythrocytes and platelets were isolated and S1P, dihydrosphingosine-1-phosphate (DHS1P), SPH, dihydrosphingosine (DHS) and CER were quantified by means of an Agilent 6460 triple quadrupole mass spectrometer using positive ion electrospray ionization source with multiple reaction monitoring. The infarction reduced the plasma level of S1P, DHS1P, SPH and DHS but increased the level of total CER. In erythrocytes, there was a sharp elevation in the level of SPH and DHS early after the infarction and a reduction after 24 h whereas the level of S1P, DHS1P and total CER gradually increased. In platelets, the level of each of the examined compounds profoundly decreased 1 and 6 h after the infarction and partially normalized in 24 h. The results obtained clearly show that experimental heart infarction in rats produces deep changes in metabolism of sphingolipids in the plasma, platelets and erythrocytes. Springer-Verlag 2012-09-09 2012 /pmc/articles/PMC3505520/ /pubmed/22961594 http://dx.doi.org/10.1007/s00395-012-0294-0 Text en © The Author(s) 2012 https://creativecommons.org/licenses/by/4.0/ This article is distributed under the terms of the Creative Commons Attribution License which permits any use, distribution, and reproduction in any medium, provided the original author(s) and the source are credited.
spellingShingle Original Contribution
Knapp, Małgorzata
Żendzian-Piotrowska, Małgorzata
Błachnio-Zabielska, Agnieszka
Zabielski, Piotr
Kurek, Krzysztof
Górski, Jan
Myocardial infarction differentially alters sphingolipid levels in plasma, erythrocytes and platelets of the rat
title Myocardial infarction differentially alters sphingolipid levels in plasma, erythrocytes and platelets of the rat
title_full Myocardial infarction differentially alters sphingolipid levels in plasma, erythrocytes and platelets of the rat
title_fullStr Myocardial infarction differentially alters sphingolipid levels in plasma, erythrocytes and platelets of the rat
title_full_unstemmed Myocardial infarction differentially alters sphingolipid levels in plasma, erythrocytes and platelets of the rat
title_short Myocardial infarction differentially alters sphingolipid levels in plasma, erythrocytes and platelets of the rat
title_sort myocardial infarction differentially alters sphingolipid levels in plasma, erythrocytes and platelets of the rat
topic Original Contribution
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3505520/
https://www.ncbi.nlm.nih.gov/pubmed/22961594
http://dx.doi.org/10.1007/s00395-012-0294-0
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