ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2009
Hemorrhagic shock augments lung endothelial cell activation: role of temporal alterations of TLR4 and TLR2.
Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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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
45 citing papers in PubMed, 77 citations in OpenAlex.
- The role of HMGB1 in vascular endothelial cells.Apoptosis : an international journal on programmed cell death · 2026Review
- Taking its TOLL: the role of toll-like receptor 4 in human health and disease, and its potential as a therapeutic target.Frontiers in immunology · 2026Review
- The Art(ery) of Contraction: Using Precision-Cut Lung Slices to Model Pulmonary Hypertension in Acute Respiratory Distress Syndrome.American journal of respiratory cell and molecular biology · 2025Article
- Navigating Hemorrhagic Shock: Biomarkers, Therapies, and Challenges in Clinical Care.Biomedicines · 2024Review
- Imaging Reactive Oxygen Radicals in Excised Mouse Lung Trapped by Reaction with Hydroxylamine Probes Using 1 GHz Rapid Scan Electron Paramagnetic Resonance.Molecular imaging and biology · 2024Article
- Cardiopulmonary Bypass Induces Acute Lung Injury via the High-Mobility Group Box 1/Toll-Like Receptor 4 Pathway.Disease markers · 2020Article
- Function and mechanism of pyrin and IL-10 in the regulation of the inflammasome in pulmonary vascular endothelial cells following hemorrhagic shock.Experimental and therapeutic medicine · 2019Article
- Use of a high platelet-to-RBC ratio of 2:1 is more effective in correcting trauma-induced coagulopathy than a ratio of 1:1 in a rat multiple trauma transfusion model.Intensive care medicine experimental · 2019Article
- Perpetual change: autophagy, the endothelium, and response to vascular injury.Journal of leukocyte biology · 2017Review
- [Association between high-mobility group box 1 and neonatal respiratory distress syndrome].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2017Article
- ROS Signaling in the Pathogenesis of Acute Lung Injury (ALI) and Acute Respiratory Distress Syndrome (ARDS).Advances in experimental medicine and biology · 2017Article
- Tlr2 on Bone Marrow and Non-Bone Marrow Derived Cells Regulates Inflammation and Organ Injury in Cooperation with Tlr4 During Resuscitated Hemorrhagic Shock.Shock (Augusta, Ga.) · 2016Article
- Resolvin D2 decreases TLR4 expression to mediate resolution in human monocytes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2016Article
- Impact of haemorrhagic shock intensity on the dynamic of alarmins release in porcine poly-trauma animal model.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2016Article
- Inhibition of peptidylarginine deiminase attenuates inflammation and improves survival in a rat model of hemorrhagic shock.The Journal of surgical research · 2016Article
- TLR2 Regulates Complement-Mediated Inflammation Induced by Blood Loss During Hemorrhage.Shock (Augusta, Ga.) · 2016Article
- Pathogenesis of infection in surgical patients.Current opinion in critical care · 2015Review
- TLR4 Deters Perfusion Recovery and Upregulates Toll-like Receptor 2 (TLR2) in Ischemic Skeletal Muscle and Endothelial Cells.Molecular medicine (Cambridge, Mass.) · 2015Article
- Hydrogen sulfide in posthemorrhagic shock mesenteric lymph drainage alleviates kidney injury in rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2015Article
- TACTIC: Trans-Agency Consortium for Trauma-Induced Coagulopathy.Journal of thrombosis and haemostasis : JTH · 2015Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
Abstract
Hemorrhagic shock (HS) due to major trauma predisposes the host to the development of acute lung inflammation and injury. The lung vascular endothelium is an active organ that plays a central role in the development of acute lung injury through generating reactive oxygen species and synthesizing and releasing of a number of inflammatory mediators, including leukocyte adhesion molecules that regulate neutrophils emigration. Previous study from our laboratory has demonstrated that in a setting of sepsis, toll-like receptor-4 (TLR4) signaling can induce TLR2 expression in endothelial cells (ECs), thereby increasing the cells' response to TLR2 ligands. The present study tested the hypothesis that TLR4 activation by HS and the resultant increased TLR2 surface expression in ECs might contribute to the mechanism underlying HS-augmented activation of lung ECs. The results show that high-mobility group box 1 (HMGB1) through TLR4 signaling mediates HS-induced surface expression of TLR2 in the lung and mouse lung vascular endothelial cells (MLVECs). Furthermore, the results demonstrate that HMGB1 induces activation of NAD(P)H oxidase and expression of ICAM-1 in the lung, and MLVECs sequentially depend on TLR4 in the early phase and on TLR2 in the late phase following HS. Finally, the data indicate an important role of the increased TLR2 surface expression in enhancing the activation of MLVECs and augmenting pulmonary neutrophil infiltration in response to TLR2 agonist peptidoglycan. Thus, induction of TLR2 surface expression in lung ECs, induced by HS and mediated by HMGB1/TLR4 signaling, is an important mechanism responsible for endothelial cell-mediated inflammation and organ injury following trauma and hemorrhage.
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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.