Evidence map›Paper›PMID 34217286›Full record

ArticleRespiratory research2021

Protectin conjugates in tissue regeneration 1 restores lipopolysaccharide-induced pulmonary endothelial glycocalyx loss via ALX/SIRT1/NF-kappa B axis.

Xin-Yang Wang, Xin-Yu Li, Cheng-Hua Wu, Yu Hao, Pan-Han Fu, Hong-Xia Mei, Fang Chen, Yu-Qiang Gong, Sheng-Wei Jin, Hui Li

Open access · goldAbstract read
In one paragraph

Article in Respiratory research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 9% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.

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  14. The Role of Histone Deacetylases in Acute Lung Injury-Friend or Foe.International journal of molecular sciences · 2023
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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

10 authors at 1 institution in 1 country.

Xin-Yang Wang *Department of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, 325027, Zhejiang, People's Republic of China.
Xin-Yu Li *Department of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, 325027, Zhejiang, People's Republic of China.
Cheng-Hua WuDepartment of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, 325027, Zhejiang, People's Republic of China.
Yu HaoDepartment of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, 325027, Zhejiang, People's Republic of China.
Pan-Han FuDepartment of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, 325027, Zhejiang, People's Republic of China.
Hong-Xia MeiDepartment of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, 325027, Zhejiang, People's Republic of China.
Fang ChenDepartment of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, 325027, Zhejiang, People's Republic of China.
Yu-Qiang GongDepartment of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, 325027, Zhejiang, People's Republic of China.
Sheng-Wei JinDepartment of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, 325027, Zhejiang, People's Republic of China. jinshengwei69@163.com.
Hui LiDepartment of Anaesthesia and Critical Care, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, 109 Xueyuan Road, Wenzhou, 325027, Zhejiang, People's Republic of China. judy198406@sina.com.ORCID http://orcid.org/0000-0003-4212-9155
Wenzhou Medical University · CN

Funding

Natural Science Foundation of Zhejiang Province LQ19H150001Natural Science Foundation of Zhejiang Province LQ20H150003Natural Science Foundation of Zhejiang Province LY19H150002Wenzhou Municipal Science and Technology Bureau Y20190087Wenzhou Municipal Science and Technology Bureau Y20190118Zhejiang Provincial Key Laboratory of Wood Science and Technology (CN) 2019C03011
6 · The paper itself

Abstract

backgroundEndothelial glycocalyx loss is integral to increased pulmonary vascular permeability in sepsis-related acute lung injury. Protectin conjugates in tissue regeneration 1 (PCTR1) is a novel macrophage-derived lipid mediator exhibiting potential anti-inflammatory and pro-resolving benefits.

methodsPCTR1 was administrated intraperitoneally with 100 ng/mouse after lipopolysaccharide (LPS) challenged. Survival rate and lung function were used to evaluate the protective effects of PCTR1. Lung inflammation response was observed by morphology and inflammatory cytokines level. Endothelial glycocalyx and its related key enzymes were measured by immunofluorescence, ELISA, and Western blot. Afterward, related-pathways inhibitors were used to identify the mechanism of endothelial glycocalyx response to PCTR1 in mice and human umbilical vein endothelial cells (HUVECs) after LPS administration.

resultsIn vivo, we show that PCTR1 protects mice against lipopolysaccharide (LPS)-induced sepsis, as shown by enhanced the survival and pulmonary function, decreased the inflammatory response in lungs and peripheral levels of inflammatory cytokines such as tumor necrosis factor-α, interleukin-6, and interleukin-1β. Moreover, PCTR1 restored lung vascular glycocalyx and reduced serum heparin sulphate (HS), syndecan-1 (SDC-1), and hyaluronic acid (HA) levels. Furthermore, we found that PCTR1 downregulated heparanase (HPA) expression to inhibit glycocalyx degradation and upregulated exostosin-1 (EXT-1) protein expression to promote glycocalyx reconstitution. Besides, we observed that BAY11-7082 blocked glycocalyx loss induced by LPS in vivo and in vitro, and BOC-2 (ALX antagonist) or EX527 (SIRT1 inhibitor) abolished the restoration of HS in response to PCTR1.

conclusionPCTR1 protects endothelial glycocalyx via ALX receptor by regulating SIRT1/NF-κB pathway, suggesting PCTR1 may be a significant therapeutic target for sepsis-related acute lung injury.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAnti-Inflammatory AgentsDocosahexaenoic AcidsGlycocalyxHumansHuman Umbilical Vein Endothelial CellsLipopolysaccharidesMaleMiceNF-kappa BRespiratory MucosaSirtuin 1Adaptor Proteins, Signal TransducingAnti-Inflammatory AgentsDocosahexaenoic AcidsHSH2 protein, mouseLipopolysaccharidesNF-kappa BSirt1 protein, mouseSirtuin 1EXT-1GlycocalyxHPAPCTR1SIRT1

Identifiers

PMID34217286
PMCPMC8254367
OpenAlexW3113591723

What OpenQuestion holds

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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.