Evidence map›Paper›PMID 25871850›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2015

Inhibition of Sphingosine Kinase 1 Ameliorates Angiotensin II-Induced Hypertension and Inhibits Transmembrane Calcium Entry via Store-Operated Calcium Channel.

Parker C Wilson, Wayne R Fitzgibbon, Sara M Garrett, Ayad A Jaffa, Louis M Luttrell, Michael W Brands, Hesham M El-Shewy

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.7field-weighted citation impact, top 16% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Role of store-operated Ca2+ entry in cardiovascular disease.Cell communication and signaling : CCS · 2022
    Review
  5. Sphingolipid Metabolism and Signaling in Endothelial Cell Functions.Advances in experimental medicine and biology · 2022
    Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. S1P Signaling and De Novo Biosynthesis in Blood Pressure Homeostasis.The Journal of pharmacology and experimental therapeutics · 2016
    Review
  14. Implication of sphingosin-1-phosphate in cardiovascular regulation.Frontiers in bioscience (Landmark edition) · 2016
    Review
  15. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 3 institutions in 2 countries.

Parker C WilsonDepartment of Pathology (P.C.W.), Yale-New Haven Hospital, New Haven, Connecticut 06510; Departments of Medicine (W.R.F., S.M.G., A.A.J., L.M.L., H.M.E.) and Biochemistry and Molecular Biology (L.M.L.), Medical University of South Carolina, Charleston, South Carolina 29425; Department of Research Service (L.M.L.), Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29401; Department of Physiology (M.W.B.), Medical College of Georgia, Georgia Health Sciences University, Augusta, Georgia 30912; and Department of Biochemistry and Molecular Genetics (A.A.J.), Faculty of Medicine, American University of Beirut, Beirut, Lebanon 113-6044.
Wayne R FitzgibbonDepartment of Pathology (P.C.W.), Yale-New Haven Hospital, New Haven, Connecticut 06510; Departments of Medicine (W.R.F., S.M.G., A.A.J., L.M.L., H.M.E.) and Biochemistry and Molecular Biology (L.M.L.), Medical University of South Carolina, Charleston, South Carolina 29425; Department of Research Service (L.M.L.), Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29401; Department of Physiology (M.W.B.), Medical College of Georgia, Georgia Health Sciences University, Augusta, Georgia 30912; and Department of Biochemistry and Molecular Genetics (A.A.J.), Faculty of Medicine, American University of Beirut, Beirut, Lebanon 113-6044.
Sara M GarrettDepartment of Pathology (P.C.W.), Yale-New Haven Hospital, New Haven, Connecticut 06510; Departments of Medicine (W.R.F., S.M.G., A.A.J., L.M.L., H.M.E.) and Biochemistry and Molecular Biology (L.M.L.), Medical University of South Carolina, Charleston, South Carolina 29425; Department of Research Service (L.M.L.), Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29401; Department of Physiology (M.W.B.), Medical College of Georgia, Georgia Health Sciences University, Augusta, Georgia 30912; and Department of Biochemistry and Molecular Genetics (A.A.J.), Faculty of Medicine, American University of Beirut, Beirut, Lebanon 113-6044.
Ayad A JaffaDepartment of Pathology (P.C.W.), Yale-New Haven Hospital, New Haven, Connecticut 06510; Departments of Medicine (W.R.F., S.M.G., A.A.J., L.M.L., H.M.E.) and Biochemistry and Molecular Biology (L.M.L.), Medical University of South Carolina, Charleston, South Carolina 29425; Department of Research Service (L.M.L.), Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29401; Department of Physiology (M.W.B.), Medical College of Georgia, Georgia Health Sciences University, Augusta, Georgia 30912; and Department of Biochemistry and Molecular Genetics (A.A.J.), Faculty of Medicine, American University of Beirut, Beirut, Lebanon 113-6044.
Louis M LuttrellDepartment of Pathology (P.C.W.), Yale-New Haven Hospital, New Haven, Connecticut 06510; Departments of Medicine (W.R.F., S.M.G., A.A.J., L.M.L., H.M.E.) and Biochemistry and Molecular Biology (L.M.L.), Medical University of South Carolina, Charleston, South Carolina 29425; Department of Research Service (L.M.L.), Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29401; Department of Physiology (M.W.B.), Medical College of Georgia, Georgia Health Sciences University, Augusta, Georgia 30912; and Department of Biochemistry and Molecular Genetics (A.A.J.), Faculty of Medicine, American University of Beirut, Beirut, Lebanon 113-6044.
Michael W BrandsDepartment of Pathology (P.C.W.), Yale-New Haven Hospital, New Haven, Connecticut 06510; Departments of Medicine (W.R.F., S.M.G., A.A.J., L.M.L., H.M.E.) and Biochemistry and Molecular Biology (L.M.L.), Medical University of South Carolina, Charleston, South Carolina 29425; Department of Research Service (L.M.L.), Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29401; Department of Physiology (M.W.B.), Medical College of Georgia, Georgia Health Sciences University, Augusta, Georgia 30912; and Department of Biochemistry and Molecular Genetics (A.A.J.), Faculty of Medicine, American University of Beirut, Beirut, Lebanon 113-6044.
Hesham M El-ShewyDepartment of Pathology (P.C.W.), Yale-New Haven Hospital, New Haven, Connecticut 06510; Departments of Medicine (W.R.F., S.M.G., A.A.J., L.M.L., H.M.E.) and Biochemistry and Molecular Biology (L.M.L.), Medical University of South Carolina, Charleston, South Carolina 29425; Department of Research Service (L.M.L.), Ralph H. Johnson Veterans Affairs Medical Center, Charleston, South Carolina 29401; Department of Physiology (M.W.B.), Medical College of Georgia, Georgia Health Sciences University, Augusta, Georgia 30912; and Department of Biochemistry and Molecular Genetics (A.A.J.), Faculty of Medicine, American University of Beirut, Beirut, Lebanon 113-6044.
Medical University of South Carolina · USAugusta University Health · USYale New Haven Hospital · US

Funding

TYROSINE KINASES IN G PROTEIN MEDIATED SIGNALINGR01DK055524 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LUTTRELL, LOUIS M · 1998 to 2017
$4.6M
MECHANISMS OF VASCULAR DISEASE IN DIABETESR01HL077192 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JAFFA, AYAD A · 2006 to 2017
$3.4M
KALLIKREIN AND VASCULAR DISEASE RISK IN DIABETESR01HL087986 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JAFFA, AYAD A · 2008 to 2011
$1.3M
Fluorometric Imaging Plate Reader (FLIPRtetra)S10RR027777 · NCRR · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LUTTRELL, LOUIS M · 2010 to 2010
$500k
KALLIKREINS-KININS AND DIABETIC VASCULAR COMPLICATIONSR01HL071255 · NHLBI · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI JAFFA, AYAD A · 2002 to 2002
$318k
Tyrosine Kinases in G Protein Mediated SignalingR56DK055524 · NIDDK · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI LUTTRELL, LOUIS M · 2008 to 2008
$284k
NCRR NIH HHS S10 RR027777NHLBI NIH HHS HL077192NHLBI NIH HHS HL087986NHLBI NIH HHS R01 HL077192NHLBI NIH HHS R01 HL087986NIDDK NIH HHS DK55524NIDDK NIH HHS R01 DK055524NIDDK NIH HHS R56 DK055524
6 · The paper itself

Abstract

Angiotensin II (AngII) plays a critical role in the regulation of vascular tone and blood pressure mainly via regulation of Ca(2+) mobilization. Several reports have implicated sphingosine kinase 1 (SK1)/sphingosine 1-phosphate (S1P) in the mobilization of intracellular Ca(2+) through a yet-undefined mechanism. Here we demonstrate that AngII-induces biphasic calcium entry in vascular smooth muscle cells, consisting of an immediate peak due to inositol tris-phosphate-dependent release of intracellular calcium, followed by a sustained transmembrane Ca(2+) influx through store-operated calcium channels (SOCs). Inhibition of SK1 attenuates the second phase of transmembrane Ca(2+) influx, suggesting a role for SK1 in AngII-dependent activation of SOC. Intracellular S1P triggers SOC-dependent Ca(2+) influx independent of S1P receptors, whereas external application of S1P stimulated S1P receptor-dependent Ca(2+) influx that is insensitive to inhibitors of SOCs, suggesting that the SK1/S1P axis regulates store-operated calcium entry via intracellular rather than extracellular actions. Genetic deletion of SK1 significantly inhibits both the acute hypertensive response to AngII in anaesthetized SK1 knockout mice and the sustained hypertensive response to continuous infusion of AngII in conscious animals. Collectively these data implicate SK1 as the missing link that connects the angiotensin AT1A receptor to transmembrane Ca(2+) influx and identify SOCs as a potential intracellular target for SK1.

Indexed as

Angiotensin IIAnimalsBlood PressureCalciumCalcium ChannelsCell MembraneChronic DiseaseEnzyme ActivationGene DeletionHEK293 CellsHumansHypertensionLysophospholipidsMaleMice, Inbred C57BLPhosphotransferases (Alcohol Group Acceptor)Angiotensin IICalciumCalcium ChannelsLysophospholipidsPhosphotransferases (Alcohol Group Acceptor)Receptors, LysosphingolipidSphingosinesphingosine 1-phosphateSphingosine Kinase

Identifiers

PMID25871850
PMCPMC4447644
OpenAlexW2170563862

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.