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Vascular transcriptome profiling identifies Sphingosine kinase 1 as a modulator of angiotensin II-induced vascular dysfunction.

ABSTRACT: Vascular dysfunction is an important phenomenon in hypertension. We hypothesized that angiotensin II (AngII) affects transcriptome in the vasculature in a region-specific manner, which may help to identify genes related to vascular dysfunction in AngII-induced hypertension. Mesenteric artery and aortic transcriptome was profiled using Illumina WG-6v2.0 chip in control and AngII infused (490?ng/kg/min) hypertensive mice. Gene set enrichment and leading edge analyses identified Sphingosine kinase 1 (Sphk1) in the highest number of pathways affected by AngII. Sphk1 mRNA, protein and activity were up-regulated in the hypertensive vasculature. Chronic sphingosine-1-phosphate (S1P) infusion resulted in a development of significantly increased vasoconstriction and endothelial dysfunction. AngII-induced hypertension was blunted in Sphk1-/- mice (systolic BP 167?±?4.2 vs. 180?±?3.3?mmHg, p?

SUBMITTER: Siedlinski M 

PROVIDER: S-EPMC5343497 | biostudies-literature | 2017 Mar

REPOSITORIES: biostudies-literature

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Vascular transcriptome profiling identifies Sphingosine kinase 1 as a modulator of angiotensin II-induced vascular dysfunction.

Siedlinski Mateusz M   Nosalski Ryszard R   Szczepaniak Piotr P   Ludwig-Gałęzowska Agnieszka H AH   Mikołajczyk Tomasz T   Filip Magdalena M   Osmenda Grzegorz G   Wilk Grzegorz G   Nowak Michał M   Wołkow Paweł P   Guzik Tomasz J TJ  

Scientific reports 20170309

Vascular dysfunction is an important phenomenon in hypertension. We hypothesized that angiotensin II (AngII) affects transcriptome in the vasculature in a region-specific manner, which may help to identify genes related to vascular dysfunction in AngII-induced hypertension. Mesenteric artery and aortic transcriptome was profiled using Illumina WG-6v2.0 chip in control and AngII infused (490 ng/kg/min) hypertensive mice. Gene set enrichment and leading edge analyses identified Sphingosine kinase  ...[more]

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