Evidence map›Paper›PMID 18927078›Full record

ArticleThe Journal of biological chemistry2008

Smooth muscle cell arachidonic acid release, migration, and proliferation are markedly attenuated in mice null for calcium-independent phospholipase A2beta.

Sung Ho Moon, Christopher M Jenkins, David J Mancuso, John Turk, Richard W Gross

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed, 36 citations in OpenAlex.

  1. Phospholipases: Where Do We Stand?Methods in molecular biology (Clifton, N.J.) · 2027
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. iPLABiochimica et biophysica acta. Molecular and cell biology of lipids · 2019
    Review
  7. The structure of iPLANature communications · 2018
    Article
  8. Cytosolic Phospholipase AInfection and immunity · 2017
    Article
  9. Lipoquality control by phospholipase AProceedings of the Japan Academy. Series B, Physical and biological sciences · 2017
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

5 authors at 1 institution in 2 countries.

Sung Ho MoonDivision of Bioorganic Chemistry and Molecular Pharmacology, Endocrinology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
Christopher M Jenkins
David J Mancuso
John Turk
Richard W Gross
Washington University in St. Louis · US

Funding

Regulation of lipid metabolism in diabetic myocardiumP01HL057278 · NHLBI · WASHINGTON UNIVERSITY · PI GROSS, RICHARD W · 1996 to 2012
$21.8M
LIPID MEDIATORS OF SIGNAL TRANSDUCTION IN SMOOTH MUSCLER01HL041250 · NHLBI · WASHINGTON UNIVERSITY · PI GROSS, RICHARD W · 1988 to 2011
$3.6M
NHLBI NIH HHS 2R01HL41250-13NHLBI NIH HHS 5P01HL57278-10
6 · The paper itself

Abstract

Pharmacologic evidence suggests that the lipid products generated by one or more calcium-independent phospholipases A(2) (iPLA(2)s) participate in the regulation of vascular tone through smooth muscle cell (SMC) Ca(2+) signaling and the release of arachidonic acid. However, the recent identification of new members of the iPLA(2) family, each inhibitable by (E)-6-(bromomethylene)-3-(1-naphthalenyl)-2H-tetrahydropyran-2-one, has rendered definitive identification of the specific enzyme(s) mediating these processes difficult. Accordingly, we used iPLA(2)beta(-/-) mice to demonstrate that iPLA(2)beta is responsible for the majority of thapsigargin and ionophore (A23187)-induced arachidonic acid release from SMCs. Both thapsigargin and A23187 stimulated robust [(3)H]arachidonate (AA) release from wild-type aortic SMCs that was dramatically attenuated in iPLA(2)beta(-/-) mice (>80% reduction at 5 min; p < 0.01). Moreover, iPLA(2)beta(-/-) mice displayed defects in SMC Ca(2+) homeostasis and decreased SMC migration and proliferation in a model of vascular injury. Ca(2+)-store depletion resulted in the rapid entry of external Ca(2+) into wild-type aortic SMCs that was significantly slower in iPLA(2)beta-null cells (p < 0.01). Furthermore, SMCs from iPLA(2)beta-null mesenteric arterial explants demonstrated decreased proliferation and migration. The defects in migration and proliferation in iPLA(2)beta-null SMCs were restored by 2 mum AA. Remarkably, the cyclooxygenase-2-specific inhibitor, NS-398, prevented AA-induced rescue of SMC migration and proliferation in iPLA(2)beta(-/-) mice. Moreover, PGE(2) alone rescued proliferation and migration in iPLA(2)beta(-/-) mice. We conclude that iPLA(2)beta is an important mediator of AA release and prostaglandin E(2) production in SMCs, modulating vascular tone, cellular signaling, proliferation, and migration.

Indexed as

AnimalsAortaArachidonic AcidCalcimycinCalciumCell MovementCell ProliferationEnzyme InhibitorsGroup IV Phospholipases A2IonophoresMiceMice, KnockoutModels, BiologicalMuscle, SmoothNitrobenzenesSulfonamidesArachidonic AcidCalcimycinCalciumEnzyme InhibitorsGroup IV Phospholipases A2IonophoresN-(2-cyclohexyloxy-4-nitrophenyl)methanesulfonamideNitrobenzenesSulfonamides

Identifiers

PMID18927078
PMCPMC2590683
OpenAlexW2148255569

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.