ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Sphingosine-1-phosphate receptor 1 agonism attenuates lung ischemia-reperfusion injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 59 citations in OpenAlex.
- Targeted immunotherapy with sphingosine-1-phosphate improves myocardial contractility and mitochondrial function in a novel murine ex vivo perfusion and transplantation model.The Journal of thoracic and cardiovascular surgery · 2025Article
- The novel compound PICCS improves cell viability during cold storage and reduces pulmonary ischemia-reperfusion injury in a rat model.Scientific reports · 2025Article
- Fingolimod Suppresses NLRP3 Inflammasome Activation and Alleviates Oxidative Stress in Traumatic Brain Injury-Induced Acute Lung Injury.Journal of inflammation research · 2025Article
- Sphingosine 1-phosphate protective effect on human proximal tubule cells submitted to an in vitro ischemia model: the role of JAK2/STAT3.Journal of physiology and biochemistry · 2024Article
- The endothelium: gatekeeper to lung ischemia-reperfusion injury.Respiratory research · 2024Review
- Dissecting the Therapeutic Mechanisms of Sphingosine-1-Phosphate Receptor Agonism during Ischaemia and Reperfusion.International journal of molecular sciences · 2023Article
- Article
- Deletion of sphingosine kinase 2 attenuates cigarette smoke-mediated chronic obstructive pulmonary disease-like symptoms by reducing lung inflammation.Biomolecules & biomedicine · 2023Article
- Signal Transduction and Gene Regulation in the Endothelium.Cold Spring Harbor perspectives in medicine · 2023Review
- Sphingosine 1-phosphate receptor-targeted therapeutics in rheumatic diseases.Nature reviews. Rheumatology · 2022Review
- Lung Biomolecular Profile and Function of Grafts from Donors after Cardiocirculatory Death with Prolonged Donor Warm Ischemia Time.Journal of clinical medicine · 2022Article
- Sphingosine 1-phosphate and its regulatory role in vascular endothelial cells.Histology and histopathology · 2022Review
- One Shoot, Two Birds: Alleviating Inflammation Caused by Ischemia/Reperfusion Injury to Reduce the Recurrence of Hepatocellular Carcinoma.Frontiers in immunology · 2022Review
- Minimizing Ischemia Reperfusion Injury in Xenotransplantation.Frontiers in immunology · 2021Review
- Impact of S1P Mimetics on Mesenteric Ischemia/Reperfusion Injury.Pharmaceuticals (Basel, Switzerland) · 2020Article
- Review 2: Primary graft dysfunction after lung transplant-pathophysiology, clinical considerations and therapeutic targets.Journal of anesthesia · 2020Review
- SPECT imaging of lung ischemia-reperfusion injury using [American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Mitochondrial transplantation enhances murine lung viability and recovery after ischemia-reperfusion injury.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- Thrombin Contributes to Anti-myeloperoxidase Antibody Positive IgG-Mediated Glomerular Endothelial Cells Activation Through SphK1-S1P-S1PR3 Signaling.Frontiers in immunology · 2019Article
- FTY720 Effects on Inflammation and Liver Damage in a Rat Model of Renal Ischemia-Reperfusion Injury.Mediators of inflammation · 2019Article
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Outcomes for lung transplantation are the worst of any solid organ, and ischemia-reperfusion injury (IRI) limits both short- and long-term outcomes. Presently no therapeutic agents are available to prevent IRI. Sphingosine 1-phosphate (S1P) modulates immune function through binding to a set of G protein-coupled receptors (S1PR1-5). Although S1P has been shown to attenuate lung IRI, the S1P receptors responsible for protection have not been defined. The present study tests the hypothesis that protection from lung IRI is primarily mediated through S1PR1 activation. Mice were treated with either vehicle, FTY720 (a nonselective S1P receptor agonist), or VPC01091 (a selective S1PR1 agonist and S1PR3 antagonist) before left lung IR. Function, vascular permeability, cytokine expression, neutrophil infiltration, and myeloperoxidase levels were measured in lungs. After IR, both FTY720 and VPC01091 significantly improved lung function (reduced pulmonary artery pressure and increased pulmonary compliance) vs. vehicle control. In addition, FTY720 and VPC01091 significantly reduced vascular permeability, expression of proinflammatory cytokines (IL-6, IL-17, IL-12/IL-23 p40, CC chemokine ligand-2, and TNF-α), myeloperoxidase levels, and neutrophil infiltration compared with control. No significant differences were observed between VPC01091 and FTY720 treatment groups. VPC01091 did not significantly affect elevated invariant natural killer T cell infiltration after IR, and administration of an S1PR1 antagonist reversed VPC01091-mediated protection after IR. In conclusion, VPC01091 and FTY720 provide comparable protection from lung injury and dysfunction after IR. These findings suggest that S1P-mediated protection from IRI is mediated by S1PR1 activation, independent of S1PR3, and that selective S1PR1 agonists may provide a novel therapeutic strategy to prevent lung IRI.
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