Evidence map›Paper›PMID 21242590›Full record

ArticleJournal of lipid research2011

Long-chain acyl-CoA synthetase 4 modulates prostaglandin E₂ release from human arterial smooth muscle cells.

Deidre L Golej, Bardia Askari, Farah Kramer, Shelley Barnhart, Anuradha Vivekanandan-Giri, Subramaniam Pennathur, Karin E Bornfeldt

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

84 citing papers in PubMed, 177 citations in OpenAlex.

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  8. Role of long-chain acyl-CoA synthetases in MASH-driven hepatocellular carcinoma and ferroptosis.American journal of physiology. Gastrointestinal and liver physiology · 2025
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24 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Deidre L GolejDepartment of Pathology, Diabetes and Obesity Center of Excellence, University of Washington School of Medicine, Seattle, WA 98109, USA.
Bardia Askari
Farah Kramer
Shelley Barnhart
Anuradha Vivekanandan-Giri
Subramaniam Pennathur
Karin E Bornfeldt
University of Washington · USUniversity of Michigan–Ann Arbor · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
Role of Serum Amyloid A in Diabetic Vascular DiseaseP01HL092969 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 2008 to 2019
$23.5M
Pilot and Feasibility (P and F) ProgramP30DK089503 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI Joyce Lee · 2010 to 2026
$20.3M
Integrated Systems Biology Approach to Diabetic Microvascular ComplicationsR24DK082841 · NIDDK · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI ABCOUWER, STEVEN F, BROSIUS, FRANK C · 2008 to 2020
$13.1M
HYPERGLYCEMIA, PROTEIN KINASES AND SMOOTH MUSCLE GROWTHR01HL062887 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 1998 to 2014
$4.7M
S100A9 and S100A8 in Diabetes and AtherosclerosisR01HL097365 · NHLBI · UNIVERSITY OF WASHINGTON · PI BORNFELDT, KARIN E. · 2010 to 2013
$1.6M
NHLBI NIH HHS HL-062887NHLBI NIH HHS HL-092969NHLBI NIH HHS HL-097365NHLBI NIH HHS P01 HL092969NHLBI NIH HHS R01 HL062887NHLBI NIH HHS R01 HL097365NIDDK NIH HHS DK-082841NIDDK NIH HHS P30 DK017047NIDDK NIH HHS P30 DK089503NIDDK NIH HHS P30 DK17047NIDDK NIH HHS R24 DK082841
6 · The paper itself

Abstract

Long-chain acyl-CoA synthetases (ACSLs) catalyze the thioesterification of long-chain FAs into their acyl-CoA derivatives. Purified ACSL4 is an arachidonic acid (20:4)-preferring ACSL isoform, and ACSL4 is therefore a probable regulator of lipid mediator production in intact cells. Eicosanoids play important roles in vascular homeostasis and disease, yet the role of ACSL4 in vascular cells is largely unknown. In the present study, the ACSL4 splice variant expressed in human arterial smooth muscle cells (SMCs) was identified as variant 1. To investigate the function of ACSL4 in SMCs, ACSL4 variant 1 was overexpressed, knocked-down by small interfering RNA, or its enzymatic activity acutely inhibited in these cells. Overexpression of ACSL4 resulted in a markedly increased synthesis of arachidonoyl-CoA, increased 20:4 incorporation into phosphatidylethanolamine, phosphatidylinositol, and triacylglycerol, and reduced cellular levels of unesterified 20:4. Accordingly, secretion of prostaglandin E₂ (PGE₂) was blunted in ACSL4-overexpressing SMCs compared with controls. Conversely, acute pharmacological inhibition of ACSL4 activity resulted in increased release of PGE₂. However, long-term downregulation of ACSL4 resulted in markedly reduced PGE₂ secretion. Thus, ACSL4 modulates PGE₂ release from human SMCs. ACSL4 may regulate a number of processes dependent on the release of arachidonic acid-derived lipid mediators in the arterial wall.

Indexed as

ArteriesBlotting, WesternCells, CulturedCoenzyme A LigasesDinoprostoneGenetic VectorsHumansIsoenzymesLong-Chain-Fatty-Acid-CoA LigaseMyocytes, Smooth MuscleRetroviridaeReverse Transcriptase Polymerase Chain ReactionCoenzyme A LigasesDinoprostoneIsoenzymesLong-Chain-Fatty-Acid-CoA Ligase

Identifiers

PMID21242590
PMCPMC3053208
OpenAlexW2113557359

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.