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• W2743123023 abstract "Ceramide accumulation in blood vessels has been attributed to vascular dysfunction in progressive vascular complications in metabolic diseases. The present study showed that ceramide pretreatment promoted PE-induced vasoconstriction in rat endothelium-denuded vascular rings in a time- and dose-dependent manner. Endoplasmic reticulum (ER) stress inhibitors, 4-PBA and TUDCA, COX-2 inhibitors, Celecoxib and NS398, as well as PGE2 receptor antagonist AH-6809 attenuated ceramide-promoted vascular hyperreactivity. Ceramide promoted the transcriptional and translational expression of COX-2 and BiP in VSMCs, which were blocked by the ER stress inhibitors, 4-PBA and TUDCA. These findings show that ceramide enhances PE-induced vascular smooth muscle constriction by mediation of the ER stress/COX-2/PGE2 pathway. Therapeutic strategies targeted to reducing ER stress and COX-2 activation might be beneficial in attenuating vascular complications.C2-Ceramide (N-acetyl-d-erythro-sphingosine) CID:2662 Tauroursodeoxycholic Acid Sodium (TUDCA) CID:9848818 phenylephrine (PE) CID:6041." @default.
• W2743123023 created "2017-08-17" @default.
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• W2743123023 date "2017-09-01" @default.
• W2743123023 modified "2023-10-14" @default.
• W2743123023 title "Ceramide enhances COX-2 expression and VSMC contractile hyperreactivity via ER stress signal activation" @default.
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• W2743123023 doi "https://doi.org/10.1016/j.vph.2017.08.001" @default.
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