Evidence map›Paper›PMID 28701173›Full record

ArticleLipids in health and disease2017

15-oxoeicosatetraenoic acid mediates monocyte adhesion to endothelial cell.

Guohua Ma, Bing Pan, Sufen Ren, Caixia Guo, Yansong Guo, Lixin Wei, Lemin Zheng, Buxing Chen

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.5field-weighted citation impact, top 35% 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

7 citing papers in PubMed, 14 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. 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

8 authors at 4 institutions in 2 countries.

Guohua MaDepartment of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, Beijing, 100050, China.
Bing PanThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Sciences of Ministry of Education, Peking University Health Science Center, Beijing, 100191, China.
Sufen RenDepartment of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, Beijing, 100050, China.
Caixia GuoDepartment of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, Beijing, 100050, China.
Yansong GuoDepartment of Cardiovascular Medicine, Fujian Provincial Hospital, Fuzhou, China.
Lixin WeiDepartment of Nephrology, Union Hospital, Fujian Medical University Union Hospital, Fuzhou, China.
Lemin ZhengThe Institute of Cardiovascular Sciences and Institute of Systems Biomedicine, School of Basic Medical Sciences, and Key Laboratory of Molecular Cardiovascular Sciences of Ministry of Education, Peking University Health Science Center, Beijing, 100191, China. zhengl@bjmu.edu.cn.
Buxing ChenDepartment of Cardiology, Beijing Tian Tan Hospital, Capital Medical University, Beijing, 100050, China. chbux@126.com.ORCID http://orcid.org/0000-0001-7473-2739
Capital Medical University · CNPeking University · CNFujian Medical University · CNFujian Provincial Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundA great number of studies reported that 12/15-lipoxygenase (12/15-LO) played an important role in atherosclerosis. And its arachidonic acid(AA) metabolite, 15(S)-hydroperoxy-5,8,11,13-(Z,Z,Z,E)-eicosatetraenoic acid (15(S)-HETE), is demonstrated to mediate endothelial dysfunction. 15-oxo-5,8,11,13-(Z,Z,Z,E)-eicosatetraenoic acid (15-oxo-ETE) was formed from 15-hydroxyprostaglandin dehydrogenase (PGDH)-mediated oxidation of 15(S)-HETE. However, relatively little is known about the biological effects of 15-oxo-ETE in cardiovascular disease. Here, we explore the likely role of 15-lipoxygenase (LO)-1-mediated AA metabolism,15-oxo-ETE, in the early pathogenesis of atherosclerosis.

methodsThe 15-oxo-ETE level in serum was detected by means of liquid chromatography and online tandem mass spectrometry (LC-MS/MS). And the underlying mechanisms were illuminated by molecular techniques, including immunoblotting, MTT assay, immunocytochemistry and Immunohistochemistry.

resultsIncreased 15-oxo-ETE level is found in in patients with acute myocardial infarction (AMI). After 15-oxo-ETE treatment, Human umbilical vein endothelial cells (HUVECs) showed more attractive to monocytes, whereas monocyte adhesion is suppressed when treated with PKC inhibitor. In ex vivo study, exposure of arteries from C57 mice and ApoE-/-mice to 15-oxo-ETE led to significantly increased E-selectin expression and monocyte adhesion.

conclusionsThis is the first report that 15-oxo-ETE promotes early pathological process of atherosclerosis by accelerating E-selectin expression and monocyte adhesion. 15-oxo-ETE -induced monocyte adhesion is partly attributable to activation of PKC.

Indexed as

AgedArachidonic AcidsCell AdhesionCell LineChromatography, LiquidEndothelial CellsFemaleHumansHuman Umbilical Vein Endothelial CellsImmunoblottingImmunohistochemistryMaleMiddle AgedMonocytesTandem Mass Spectrometry15-oxo-5,8,11,13-eicosatetraenoic acidArachidonic Acids15-oxo-ETEAtherosclerosisE-selectinmonocyte adhesionPKC

Identifiers

PMID28701173
PMCPMC5508789
OpenAlexW2735797894

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.