ArticleRedox biology2017
Resolvin D1 via prevention of ROS-mediated SHP2 inactivation protects endothelial adherens junction integrity and barrier function.
Article in Redox biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 61 citations in OpenAlex.
- Role of long-chain polyunsaturated fatty acids, eicosapentaenoic and docosahexaenoic, in the regulation of gene expression during the development of obesity: a systematic review.Frontiers in nutrition · 2023Pooled it
- G protein-coupled receptors and inflammation resolution signaling networks in the heart: Pharmacology and potential for innovative therapeutics.Pharmacological reviews · 2026Review
- Endothelial barrier and sepsis: mechanisms and potential therapeutic strategies.Military Medical Research · 2026Review
- Reactive Oxygen Species: A Double-Edged Sword in the Modulation of Cancer Signaling Pathway Dynamics.Cells · 2025Review
- 15-PGDH inhibition preserves blood-brain barrier integrity and cognition.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Anti-Inflammatory Lipid Mediators from Polyunsaturated Fatty Acids: Insights into their Role in Atherosclerosis Microenvironments.Current atherosclerosis reports · 2025Review
- The potential of exogenous specialized pro-resolving mediators in protecting against sepsis-associated lung injury: a review.Frontiers in pharmacology · 2025Review
- MSU crystallization promotes fibroblast proliferation and renal fibrosis in diabetic nephropathy via the ROS/SHP2/TGFβ pathway.Scientific reports · 2024Article
- Application of Antioxidant Compounds in Bone Defect Repair.Antioxidants (Basel, Switzerland) · 2024Review
- Resolving neutrophils through genetic deletion of TRAM attenuate atherosclerosis pathogenesis.iScience · 2024Article
- Article
- Article
- Polyunsaturated Fatty Acids: Conversion to Lipid Mediators, Roles in Inflammatory Diseases and Dietary Sources.International journal of molecular sciences · 2023Review
- Inhibition of fatty acid synthase protects obese mice from acute lung injury via ameliorating lung endothelial dysfunction.Respiratory research · 2023Article
- Classes of Lipid Mediators and Their Effects on Vascular Inflammation in Atherosclerosis.International journal of molecular sciences · 2023Review
- The Impact of Resolution of Inflammation on Tumor Microenvironment: Exploring New Ways to Control Cancer Progression.Cancers · 2022Review
- Epithelial-mesenchymal transition: The history, regulatory mechanism, and cancer therapeutic opportunities.MedComm · 2022Review
- Resolution-promoting autacoids demonstrate promising cardioprotective effects against heart diseases.Molecular biology reports · 2022Review
- Unexpected Role of MPO-Oxidized LDLs in Atherosclerosis: In between Inflammation and Its Resolution.Antioxidants (Basel, Switzerland) · 2022Review
- Generation of resolving memory neutrophils through pharmacological training with 4-PBA or genetic deletion of TRAM.Cell death & disease · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Resolvins are a novel class of lipid mediators that play an important role in the resolution of inflammation, although the underlying mechanisms are not very clear. To explore the anti-inflammatory mechanisms of resolvins, we have studied the effects of resolvin D1 (RvD1) on lipopolysaccharide (LPS)-induced endothelial barrier disruption as it is linked to propagation of inflammation. We found that LPS induces endothelial cell (EC) barrier disruption via xanthine oxidase (XO)-mediated reactive oxygen species (ROS) production, protein tyrosine phosphatase SHP2 inactivation and Fyn-related kinase (Frk) activation leading to tyrosine phosphorylation of α-catenin and VE-cadherin and their dissociation from each other affecting adherens junction (AJ) integrity and thereby increasing endothelial barrier permeability. RvD1 attenuated LPS-induced AJ disassembly and endothelial barrier permeability by arresting tyrosine phosphorylation of α-catenin and VE-cadherin and their dislocation from AJ via blockade of XO-mediated ROS production and thereby suppression of SHP2 inhibition and Frk activation. We have also found that the protective effects of RvD1 on EC barrier function involve ALX/FPR2 and GPR32 as inhibition or neutralization of these receptors negates its protective effects. LPS also increased XO activity, SHP2 cysteine oxidation and its inactivation, Frk activation, α-catenin and VE-cadherin tyrosine phosphorylation and their dissociation from each other leading to AJ disruption with increased vascular permeability in mice arteries and RvD1 blocked all these effects. Thus, RvD1 protects endothelial AJ and its barrier function from disruption by inflammatory mediators such as LPS via a mechanism involving the suppression of XO-mediated ROS production and blocking SHP2 inactivation.
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Registered trials
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.