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Total 26 results found since Jan 2013.

Histone Deacetylase 7 Inhibition in a Murine Model of Gram-Negative Pneumonia-Induced Acute Lung Injury
Conclusion: HDAC7 appears to play a key role in the inflammatory response that leads to ALI after gram-negative pneumonia in mice.
Source: Shock - February 12, 2020 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

Herpes Virus Entry Mediator (HVEM) Expression Promotes Inflammation/ Organ Injury in Response to Experimental Indirect-Acute Lung Injury
Therapeutic interventions to treat acute lung injury (ALI) remain largely limited to lung-protective strategies, as a real molecular pathophysiologically driven therapeutic intervention has yet to become available. While we have previously documented the expression of herpes virus entry mediator (HVEM) on leukocytes of septic mice and critically ill patients, its functional role in shock/sepsis-induced ALI has not yet been studied. Inasmuch, a murine model of indirect ALI (iALI) was induced by hemorrhagic shock (HEM) followed by cecal ligation and puncture (CLP), septic challenge and HVEM-siRNA or phosphate buffered saline...
Source: Shock - March 14, 2019 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

Patho-Mechanisms for Hemorrhage/Sepsis-Induced Indirect Acute Respiratory Distress Syndrome: A Role for Lung TIE1 and Its Regulation by Neutrophils
Conclusion: Together, these data imply that shock-induced increased expression of Tie1 can contribute to EC activation by inhibiting Ang:Tie2 interaction, culminating in EC dysfunction and the development of iARDS.
Source: Shock - March 16, 2022 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

The wnk4/spak pathway stimulates alveolar fluid clearance by upregulation of epithelial sodium channel in mice with lipopolysaccharide-induced acute respiratory distress syndrome
With-No lysine Kinases (WNKs) have been newly implicated in alveolar fluid clearance (AFC). Epithelial sodium channels (ENaCs) serve a vital role in AFC. The potential protective effect of WNK4 in acute respiratory distress syndrome (ARDS), mediated by ENaC-associated AFC was investigated in the study. A model of lipopolysaccharide (LPS)-induced ARDS was established in C57BL/6 mice. WNK4, Sterile 20-related proline-alanine-rich kinase (SPAK), small interfering RNA (siRNA)-WNK4 or siRNA-SPAK were transfected into mouse lung or primary alveolar epithelial type II (ATII) cells. AFC, bronchoalveolar lavage fluid and lung histo...
Source: Shock - July 1, 2022 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

Drug Repurposing Screen Identifies Foxo1-Dependent Angiopoietin-2 Regulation in Sepsis*
Conclusions: 3-hydroxy-3-methyl-glutaryl-CoA reductase inhibitors may operate through a novel Foxo1-angiopoietin-2 mechanism to suppress de novo production of angiopoietin-2 and thereby ameliorate manifestations of sepsis. Given angiopoietin-2’s dual role as a biomarker and candidate disease mediator, early serum angiopoietin-2 measurement may serve as a stratification tool for future trials of drugs targeting vascular leakage.
Source: Critical Care Medicine - June 17, 2015 Category: Emergency Medicine Tags: Online Laboratory Investigations Source Type: research

Endocytosis of Red Blood Cell Microparticles by Pulmonary Endothelial Cells is Mediated By Rab5
Microparticles are submicron vesicles shed from aging erythrocytes as a characteristic feature of the red blood cell (RBC) storage lesion. Exposure of pulmonary endothelial cells to RBC-derived microparticles promotes an inflammatory response, but the mechanisms underlying microparticle-induced endothelial cell activation are poorly understood. In the present study, cultured murine lung endothelial cells (MLECs) were treated with microparticles isolated from aged murine packed RBCs or vehicle. Microparticle-treated cells demonstrated increased expression of the adhesion molecules ICAM and E-selectin, as well as the cytokin...
Source: Shock - February 14, 2018 Category: Emergency Medicine Tags: 2017 New Investigator Award Competition Source Type: research

Endoplasmic Reticulum Stress-Induced NLRP1 Inflammasome Activation Contributes to Myocardial Ischemia/Reperfusion Injury
In conclusion, NLRP1 inflammasome activation promotes myocardial I/R injury. ER stress can activate NLRP1 inflammasome via activating the NF-κB signaling pathway.
Source: Shock - March 14, 2019 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

DC-SIGN Expression in Intestinal Epithelial Cells Regulates Sepsis-Associated Acute Intestinal Injury Via Activating ERK1/2-NF-κB/P65 Signaling
Conclusions: Sepsis-induced DC-SIGN expression in IECs plays a significant role in regulating acute intestinal injury and systemic inflammatory response. The inhibition of DC-SIGN exhibited protective effects on sepsis-associated organ injury and systemic inflammation.
Source: Shock - September 17, 2019 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

Stem Cell Therapy and Hydrogen Sulfide: Conventional or Nonconventional Mechanisms of Action?
Conclusions: Knocking down conventional H2S-producing enzymes only impacted gas production in normoxic conditions. When cells were transfected in hypoxic conditions, as would be expected in the ischemic intestines, H2S gas was not depressed. These data, along with unchanged perfusion and histological injury parameters with conventional enzyme knockdown, would indicate that alternative H2S production pathways may be initiated during hypoxic and/or ischemic events.
Source: Shock - May 16, 2020 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

MEF2D Participates in Microglia-Mediated Neuroprotection in Cerebral Ischemia-Reperfusion Rats
Conclusion: These results indicate that MEF2D is a necessary molecule for neuroinflammation regulation and neuronal injury in cerebral ischemia.
Source: Shock - December 17, 2021 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

Activation of the mitochondrial antiviral signaling protein (mavs) following liver ischemia/reperfusion and its effect on inflammation and injury
Resuscitation of trauma patients after hemorrhagic shock causes global I/R, which may contribute to organ dysfunction. Oxidative stress resulting from I/R is known to induce signaling pathways leading to the production of inflammatory molecules culminating in organ dysfunction/injury. Our recent work demonstrated that oxidative stress was able to induce activation of the mitochondrial antiviral signaling protein (MAVS), a protein known to be involved in antiviral immunity, in an in vitro model. We therefore hypothesized that the MAVS pathway might be involved in I/R-induced inflammation and injury. The present studies show...
Source: Shock - July 1, 2022 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

Novel Role of Resveratrol: Suppression of High-Mobility Group Protein Box 1 Nucleocytoplasmic Translocation by the Upregulation of Sirtuin 1 in Sepsis-Induced Liver Injury
Conclusions: Resveratrol protects against sepsis-induced liver injury through the SIRT1-mediated HMGB1 nucleocytoplasmic translocation pathway, a new potential therapeutic target in sepsis-induced liver injury.
Source: Shock - October 17, 2014 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

Fluorofenidone Attenuates TGF-β1–Induced Lung Fibroblast Activation via Restoring the Expression of Caveolin-1
In this study, we explore mainly whether caveolin-1 plays a critical role in the anti–pulmonary fibrosis effects of FD in vitro. The normal human lung fibroblasts (NHLFs) were cultured with transforming growth factor-β1 (TGF-β1) and then were treated with FD. Subsequently, NHLFs transfected with cav-1-siRNA were treated with TGF-β1 and/or FD. The expressions of α-smooth muscle actin (α-SMA), fibronectin, collagen I, caveolin-1, phosphorylated extracellular signal–regulated kinase (p-ERK), phosphorylated c-Jun N-terminal kinase (p-JNK), and phosphorylated P38 were measured by Western blot and/or real-time polymeras...
Source: Shock - January 24, 2015 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research

Progranulin Reduced Neuronal Cell Death by Activation of Sortilin 1 Signaling Pathways After Subarachnoid Hemorrhage in Rats
Conclusion: Rat recombinant progranulin alleviated neuronal death via sortilin 1-mediated and Akt-related antiapoptosis pathway. Rat recombinant progranulin may have potentials to ameliorate early brain injury for subarachnoid hemorrhage patients.
Source: Critical Care Medicine - July 17, 2015 Category: Emergency Medicine Tags: Online Laboratory Investigations Source Type: research

Vitamin C Attenuates Hemorrhagic Hypotension Induced Epithelial–Dendritic Cell Transformation in Rat Intestines by Maintaining GSK-3β Activity and E-Cadherin Expression
Conclusions: HH induces EDT in rat intestine epithelial cells. VitC maintains GSK-3β activity, attenuates the suppression of E-cadherin caused by hypoxia, and ultimately decreases DC-SIGN expression.
Source: Shock - December 18, 2015 Category: Emergency Medicine Tags: Basic Science Aspects Source Type: research