Acyl chain-dependent effect of lysophosphatidylcholine on endothelium-dependent vasorelaxation.
Previously we identified palmitoyl-, oleoyl-, linoleoyl-, and arachidonoyl-lysophosphatidylcholine (LPC 16:0, 18:1, 18:2 and 20:4) as the most prominent LPC species generated by endothelial lipase (EL). In the present study, we examined the impact of those LPC on acetylcholine (ACh)- induced vascula...
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2013-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3669280?pdf=render |
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| author | Shailaja P Rao Monika Riederer Margarete Lechleitner Martin Hermansson Gernot Desoye Seth Hallström Wolfgang F Graier Saša Frank |
| author_facet | Shailaja P Rao Monika Riederer Margarete Lechleitner Martin Hermansson Gernot Desoye Seth Hallström Wolfgang F Graier Saša Frank |
| author_sort | Shailaja P Rao |
| collection | DOAJ |
| description | Previously we identified palmitoyl-, oleoyl-, linoleoyl-, and arachidonoyl-lysophosphatidylcholine (LPC 16:0, 18:1, 18:2 and 20:4) as the most prominent LPC species generated by endothelial lipase (EL). In the present study, we examined the impact of those LPC on acetylcholine (ACh)- induced vascular relaxation. All tested LPC attenuated ACh-induced relaxation, measured ex vivo, using mouse aortic rings and wire myography. The rank order of potency was as follows: 18:2>20:4>16:0>18:1. The attenuating effect of LPC 16:0 on relaxation was augmented by indomethacin-mediated cyclooxygenase (COX)-inhibition and CAY10441, a prostacyclin (PGI2)- receptor (IP) antagonist. Relaxation attenuated by LPC 20:4 and 18:2 was improved by indomethacin and SQ29548, a thromboxane A2 (TXA2)- receptor antagonist. The effect of LPC 20:4 could also be improved by TXA2- and PGI2-synthase inhibitors. As determined by EIA assays, the tested LPC promoted secretion of PGI2, TXA2, PGF2α, and PGE2, however, with markedly different potencies. LPC 16:0 was the most potent inducer of superoxide anion production by mouse aortic rings, followed by LPC 18:2, 20:4 and 18:1, respectively. The strong antioxidant tempol recovered relaxation impairment caused by LPC 18:2, 18:1 and 20:4, but not by LPC 16:0. The tested LPC attenuate ACh-induced relaxation through induction of proconstricting prostanoids and superoxide anions. The potency of attenuating relaxation and the relative contribution of underlying mechanisms are strongly related to LPC acyl-chain length and degree of saturation. |
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| id | doaj.art-17b6b528d4b74f3dab7ff790d2194a99 |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-20T06:32:20Z |
| publishDate | 2013-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-17b6b528d4b74f3dab7ff790d2194a992022-12-21T19:50:06ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-0185e6515510.1371/journal.pone.0065155Acyl chain-dependent effect of lysophosphatidylcholine on endothelium-dependent vasorelaxation.Shailaja P RaoMonika RiedererMargarete LechleitnerMartin HermanssonGernot DesoyeSeth HallströmWolfgang F GraierSaša FrankPreviously we identified palmitoyl-, oleoyl-, linoleoyl-, and arachidonoyl-lysophosphatidylcholine (LPC 16:0, 18:1, 18:2 and 20:4) as the most prominent LPC species generated by endothelial lipase (EL). In the present study, we examined the impact of those LPC on acetylcholine (ACh)- induced vascular relaxation. All tested LPC attenuated ACh-induced relaxation, measured ex vivo, using mouse aortic rings and wire myography. The rank order of potency was as follows: 18:2>20:4>16:0>18:1. The attenuating effect of LPC 16:0 on relaxation was augmented by indomethacin-mediated cyclooxygenase (COX)-inhibition and CAY10441, a prostacyclin (PGI2)- receptor (IP) antagonist. Relaxation attenuated by LPC 20:4 and 18:2 was improved by indomethacin and SQ29548, a thromboxane A2 (TXA2)- receptor antagonist. The effect of LPC 20:4 could also be improved by TXA2- and PGI2-synthase inhibitors. As determined by EIA assays, the tested LPC promoted secretion of PGI2, TXA2, PGF2α, and PGE2, however, with markedly different potencies. LPC 16:0 was the most potent inducer of superoxide anion production by mouse aortic rings, followed by LPC 18:2, 20:4 and 18:1, respectively. The strong antioxidant tempol recovered relaxation impairment caused by LPC 18:2, 18:1 and 20:4, but not by LPC 16:0. The tested LPC attenuate ACh-induced relaxation through induction of proconstricting prostanoids and superoxide anions. The potency of attenuating relaxation and the relative contribution of underlying mechanisms are strongly related to LPC acyl-chain length and degree of saturation.http://europepmc.org/articles/PMC3669280?pdf=render |
| spellingShingle | Shailaja P Rao Monika Riederer Margarete Lechleitner Martin Hermansson Gernot Desoye Seth Hallström Wolfgang F Graier Saša Frank Acyl chain-dependent effect of lysophosphatidylcholine on endothelium-dependent vasorelaxation. PLoS ONE |
| title | Acyl chain-dependent effect of lysophosphatidylcholine on endothelium-dependent vasorelaxation. |
| title_full | Acyl chain-dependent effect of lysophosphatidylcholine on endothelium-dependent vasorelaxation. |
| title_fullStr | Acyl chain-dependent effect of lysophosphatidylcholine on endothelium-dependent vasorelaxation. |
| title_full_unstemmed | Acyl chain-dependent effect of lysophosphatidylcholine on endothelium-dependent vasorelaxation. |
| title_short | Acyl chain-dependent effect of lysophosphatidylcholine on endothelium-dependent vasorelaxation. |
| title_sort | acyl chain dependent effect of lysophosphatidylcholine on endothelium dependent vasorelaxation |
| url | http://europepmc.org/articles/PMC3669280?pdf=render |
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