Evidence map›Paper›PMID 19433984›Full record

ArticleJournal of cardiovascular pharmacology2009

Cardiomyocyte S1P1 receptor-mediated extracellular signal-related kinase signaling and desensitization.

Rong Tao, Holly E Hoover, Jianqing Zhang, Norman Honbo, Conrad C Alano, Joel S Karliner

Open access · greenAbstract read
In one paragraph

Article in Journal of cardiovascular pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.7field-weighted citation impact, top 17% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. You aren't IMMUNE to the ceramides that accumulate in cardiometabolic disease.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2022
    Article
  2. Article
  3. Implication of sphingosin-1-phosphate in cardiovascular regulation.Frontiers in bioscience (Landmark edition) · 2016
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Multiple sclerosis: the role of cytokines in pathogenesis and in therapies.International journal of molecular sciences · 2012
    Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. S1P lyase: a novel therapeutic target for ischemia-reperfusion injury of the heart.American journal of physiology. Heart and circulatory physiology · 2011
    Article
  15. Article
  16. Article
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

6 authors at 3 institutions in 2 countries.

Rong TaoDepartment of Medicine, Veterans Affairs Medical Center, University of California, San Francisco, CA 94121, USA.
Holly E Hoover
Jianqing Zhang
Norman Honbo
Conrad C Alano
Joel S Karliner
University of California, San Francisco · USSan Francisco VA Medical Center · USVeterans Health Administration · US

Funding

Mechanisms of Cardioprotection in Ischemia and FailureP01HL068738 · NHLBI · NORTHERN CALIFORNIA INSTITUTE RES &EDUC · PI KARLINER, JOEL SAMUEL · 2002 to 2006
$8.6M
NHLBI NIH HHS 1P01 HL068738-01A1NHLBI NIH HHS P01 HL068738
6 · The paper itself

Abstract

We examined the ability of sphingosine-1-phosphate (S1P) to desensitize extracellular signal-related kinase (ERK), a mitogen-activated protein kinase linked to antiapoptotic responses in the heart. In isolated adult mouse cardiomyocytes, S1P (10 nM-5 microM) induced ERK phosphorylation in a time- and dose-dependent manner. S1P stimulation of ERK was completely inhibited by an S1P1/3 subtype receptor antagonist (VPC23019), by a Gi protein inhibitor (pertussis toxin) and by a mitogen-activated protein kinase/ERK kinase inhibitor (PD98059). A selective S1P3 receptor antagonist (CAY10444) had no effect on S1P-induced ERK activation. The selective S1P1 agonist SEW2871 also induced ERK phosphorylation. Activation of ERK by restimulation with 100 nM S1P was suppressed after 1 hour of preincubation with 100 nM S1P but recovered fully the next day, suggesting receptor recycling. Similar results were obtained in protein kinase C epsilon-null cardiomyocytes. Treatment with the nonselective S1P receptor agonist FTY720 for 1 hour also reduced phospho-ERK expression in response to subsequent S1P stimulation. In contrast to S1P, some desensitization to FTY720 persisted after overnight exposure. Cell death induced by hypoxia/reoxygenation was reduced by pretreatment with exogenous S1P. This enhanced survival was abrogated by pretreatment with PD98059, VPC23019, or pertussis toxin. Thus, exogenous S1P induces rapid and reversible S1P1-mediated ERK phosphorylation. S1P-induced adult mouse cardiomyocyte survival requires ERK activation mediated via an S1P1-Gi pathway.

Indexed as

AnimalsCell DeathCell HypoxiaCells, CulturedCell SurvivalEnzyme ActivationExtracellular Signal-Regulated MAP KinasesIn Vitro TechniquesLysophospholipidsMaleMiceMice, Inbred C57BLMice, KnockoutMyocytes, CardiacPhosphorylationProtein Kinase CCAY10444Extracellular Signal-Regulated MAP KinasesLysophospholipidsProtein Kinase CReceptors, LysosphingolipidSphingosinesphingosine 1-phosphateThiazolidines

Identifiers

PMID19433984
PMCPMC2835551
OpenAlexW1980654851

What OpenQuestion holds

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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.