Evidence map›Paper›PMID 32123295›Full record

ArticleLaboratory investigation; a journal of technical methods and pathology2020

PCTR1 ameliorates lipopolysaccharide-induced acute inflammation and multiple organ damage via regulation of linoleic acid metabolism by promoting FADS1/FASDS2/ELOV2 expression and reducing PLA2 expression.

Yong-Jian Liu, Hui Li, Yang Tian, Jun Han, Xin-Yang Wang, Xin-Yu Li, Chao Tian, Pu-Hong Zhang, Yu Hao, Fang Gao and 1 more

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Article in Laboratory investigation; a journal of technical methods and pathology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

18 citing papers in PubMed, 1 synthesis or guideline pooled it.

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  16. PCTR1 Enhances Repair and Bacterial Clearance in Skin Wounds.The American journal of pathology · 2021
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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

11 authors.

Yong-Jian LiuDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China.
Hui LiDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China.
Yang TianDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China.
Jun HanDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China.
Xin-Yang WangDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China.
Xin-Yu LiDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China.
Chao TianDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China.
Pu-Hong ZhangDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China.
Yu HaoDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China. haoyu8403@163.com.
Fang GaoDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China. f.gaosmith@bham.ac.uk.
Sheng-Wei JinDepartment of Anaesthesia and Critical Care, the Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 325027, Zhejiang, PR China. jinshengwei69@163.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gram-negative bacterial infection causes an excessive inflammatory response and acute organ damage or dysfunction due to its outer membrane component, lipopolysaccharide (LPS). Protectin conjugates in tissue regeneration 1 (PCTR1), an endogenous lipid mediator, exerts fundamental anti-inflammation and pro-resolution during infection. In the present study, we examined the properties of PCTR1 on the systemic inflammatory response, organic morphological damage and dysfunction, and serum metabolic biomarkers in an LPS-induced acute inflammatory mouse model. The results show that PCTR1 reduced serum inflammatory factors and ameliorated morphological damage and dysfunction of the lung, liver, kidney, and ultimately improved the survival rate of LPS-induced acute inflammation in mice. In addition, metabolomics analysis and high performance liquid chromatography-mass spectrometry revealed that LPS-stimulated serum linoleic acid (LA), arachidonic acid (AA), and prostaglandin E2 (PGE2) levels were significantly altered by PCTR1. Moreover, PCTR1 upregulated LPS-inhibited fatty acid desaturase 1 (FADS1), fatty acid desaturase 2 (FADS2), and elongase of very long chain fatty acids 2 (ELOVL2) expression, and downregulated LPS-stimulated phospholipase A2 (PLA2) expression to increase the intrahepatic content of AA. However, these effects of PCTR1 were partially abrogated by a lipoxin A4 receptor (ALX) antagonist (BOC-2). In summary, via the activation of ALX, PCTR1 promotes the conversion of LA to AA through upregulation of FADS1, FADS2, and ELOVL2 expression, and inhibits the conversion of bound AA into free AA through downregulation of PLA2 expression to decrease the serum AA and PGE2 levels.

Indexed as

AnimalsCD59 AntigensDocosahexaenoic AcidsFatty Acid DesaturasesFatty Acid ElongasesFemaleInflammationLinoleic AcidLipid MetabolismLipopolysaccharidesMaleMiceMice, Inbred C57BLPhospholipases A217-hydroxy-4,7,10,13,15,19-docosahexaenoic acidCD59 AntigensDocosahexaenoic AcidsFADS1 protein, mouseFADS2 protein, mouseFatty Acid DesaturasesFatty Acid ElongasesLinoleic AcidLipopolysaccharidesPhospholipases A2

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Registered trials

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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.