ArticleBritish journal of pharmacology2006
Sphingolipids differentially regulate mitogen-activated protein kinases and intracellular Ca2+ in vascular smooth muscle: effects on CREB activation.
Article in British journal of pharmacology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- SPTLC3 regulates plasma membrane sphingolipid composition to facilitate hepatic gluconeogenesis.Cell reports · 2024Article
- Proteomic-Based Approach Reveals the Involvement of Apolipoprotein A-I in Related Phenotypes of Autism Spectrum Disorder in the BTBR Mouse Model.International journal of molecular sciences · 2022Article
- The dynamics and role of sphingolipids in eukaryotic organisms upon thermal adaptation.Progress in lipid research · 2020Review
- Comparative Proteomic Analysis ofInternational journal of molecular sciences · 2019Article
- Emerging roles of sphingosylphosphorylcholine in modulating cardiovascular functions and diseases.Acta pharmacologica Sinica · 2018Review
- Sphingosylphosphorylcholine inhibits macrophage adhesion to vascular smooth muscle cells.Biochemical pharmacology · 2016Article
- Ginsenoside Rg1 attenuates hypoxia and hypercapnia-induced vasoconstriction in isolated rat pulmonary arterial rings by reducing the expression of p38.Journal of thoracic disease · 2016Article
- Sphingosylphosphorylcholine potentiates vasoreactivity and voltage-gated Ca2+ entry via NOX1 and reactive oxygen species.Cardiovascular research · 2015Article
- Sphingosine-1-phosphate rapidly increases cortisol biosynthesis and the expression of genes involved in cholesterol uptake and transport in H295R adrenocortical cells.Molecular and cellular endocrinology · 2012Article
- Apoptotic cell-derived factors induce arginase II expression in murine macrophages by activating ERK5/CREB.Cellular and molecular life sciences : CMLS · 2011Article
- S1P activates store-operated calcium entry via receptor- and non-receptor-mediated pathways in vascular smooth muscle cells.American journal of physiology. Cell physiology · 2011Article
- Sphingosylphosphorylcholine is a proinflammatory mediator in cerebral arteries.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2011Article
- The impact of bioactive lipids on cardiovascular development.Stem cells international · 2011Article
- Sphingosine-1-phosphate signaling in vasculogenesis and angiogenesis.World journal of biological chemistry · 2010Article
- Development of a sphingosylphosphorylcholine detection system using RNA aptamers.Molecules (Basel, Switzerland) · 2010Article
- Intravenous sphingosylphosphorylcholine protects ischemic and postischemic myocardial tissue in a mouse model of myocardial ischemia/reperfusion injury.Mediators of inflammation · 2010Article
- Sphingolipids in inflammation: pathological implications and potential therapeutic targets.British journal of pharmacology · 2009Review
- Human neural progenitors express functional lysophospholipid receptors that regulate cell growth and morphology.BMC neuroscience · 2008Article
- Membranes: a meeting point for lipids, proteins and therapies.Journal of cellular and molecular medicine · 2008Review
- Indomethacin differentiates the renal effects of sphingosine-1-phosphate and sphingosylphosphorylcholine.Naunyn-Schmiedeberg's archives of pharmacology · 2006Article
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2 authors at 2 institutions in 2 countries.
Funding
Abstract
1. Related sphingolipids, sphingosine 1-phosphate (S1P) and sphingosylphosphorylcholine (SPC), have important effects on vascular smooth muscle. The aim of this study was to investigate the intracellular pathways regulated by S1P and SPC in rat cerebral artery. 2. In cerebral arteries, S1P increased extracellular signal-regulated kinase (ERK)1/2 phosphorylation (5.2+/-1.4-fold increase) but did not activate p38 mitogen-activated protein kinase (p38MAPK) as assessed by immunoblotting. In contrast, SPC increased p38MAPK phosphorylation (3.0+/-0.3-fold increase) but did not stimulate ERK1/2. This differential activation was confirmed by measuring activation of heat shock protein (HSP) 27, a known downstream target of p38MAPK. Only SPC, but not S1P, activated HSP27. 3. In enzymatically dispersed cerebral artery myocytes, SPC increased [Ca2+]i in a concentration-dependent manner (peak response at 10 microM: 0.4+/-0.02 ratio units) as determined using the Ca2+ indicator, Fura 2. In contrast to S1P, the SPC-induced [Ca2+]i increase did not involve intracellular release but was due to Ca2+ influx via L-type Ca2+ channels. 4. Despite differences in signalling, both S1P and SPC phosphorylated the transcription factor cAMP response element-binding protein (CREB). S1P-induced CREB activation was dependent on ERK1/2 and Ca2+-calmodulin-dependent protein kinase (CaMK) activation. CREB activation by SPC required both p38MAPK and CaMK activation, but not ERK1/2. 5. In conclusion, S1P and SPC activate distinct MAP kinase isoforms and increase [Ca2+]i via different mechanisms in rat cerebral artery. This does not affect the ability of S1P or SPC to activate CREB, although this occurs via different pathways.
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