Roles of RAGE/ROCK1 Pathway in HMGB1-Induced Early Changes in Barrier Permeability of Human Pulmonary Microvascular Endothelial Cell

Zhao, Mengsheng; Jiang, Haoran; Sun, Jingwen; Wang, Ziang; Hu, Bo; Zhu, Chengrui; Yin, Xiaohan; Chen, Mingming; Ma, Xiaochun; Zhao, Weidong; Luan, Zhenggang

doi:10.3389/fimmu.2021.697071

Cited by 18 publications

(16 citation statements)

References 37 publications

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“…Notably, the blockade of RAGE using sRAGE attenuated the Ang II-induced increase in endothelial hyperpermeability (Jeong et al, 2019). A recent study reported similar findings regarding the HMGB-1-RAGE axis enhancing barrier permeability in human pulmonary microvascular endothelial cells (Zhao et al, 2021). Sepsis-associated acute kidney injury is a common complication in hospitalized and critically ill patients.…”

Section: Rage Mediates Endothelial Permeability In Diabetic Conditionsmentioning

confidence: 70%

RAGE signaling regulates the progression of diabetic complications

Taguchi

Fukami

2023

Front. Pharmacol.

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Diabetes, the ninth leading cause of death globally, is expected to affect 642 million people by 2040. With the advancement of an aging society, the number of patients with diabetes having multiple underlying diseases, such as hypertension, obesity, and chronic inflammation, is increasing. Thus, the concept of diabetic kidney disease (DKD) has been accepted worldwide, and comprehensive treatment of patients with diabetes is required. Receptor for advanced glycation endproducts (RAGE), a multiligand receptor, belonging to the immunoglobulin superfamily is extensively expressed throughout the body. Various types of ligands, including advanced glycation endproducts (AGEs), high mobility group box 1, S100/calgranulins, and nucleic acids, bind to RAGE, and then induces signal transduction to amplify the inflammatory response and promote migration, invasion, and proliferation of cells. Furthermore, the expression level of RAGE is upregulated in patients with diabetes, hypertension, obesity, and chronic inflammation, suggesting that activation of RAGE is a common denominator in the context of DKD. Considering that ligand–and RAGE–targeting compounds have been developed, RAGE and its ligands can be potent therapeutic targets for inhibiting the progression of DKD and its complications. Here, we aimed to review recent literature on various signaling pathways mediated by RAGE in the pathogenesis of diabetic complications. Our findings highlight the possibility of using RAGE–or ligand–targeted therapy for treating DKD and its complications.

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Section: Rage Mediates Endothelial Permeability In Diabetic Conditionsmentioning

confidence: 70%

RAGE signaling regulates the progression of diabetic complications

Taguchi

Fukami

2023

Front. Pharmacol.

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“…Disulfide-HMGB1 secreted can then potentially mediate a positive feedback loop by binding to TLR4 and initiating a downstream pro-inflammatory signaling cascade, which can further induce cell death. In addition, HMGB1 disrupts the integrity of the endothelial barrier through the advanced glycation end products/Rho-associated kinase 1 pathway, which induces stress fiber formation in the short term via phosphorylation of the myosin light chain [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Association between serum HMGB1 elevation and early pediatric acute respiratory distress syndrome: a retrospective study of pediatric living donor liver transplant recipients with biliary atresia in China

et al. 2023

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Background High mobility group box 1 (HMGB1) protein is one of the main risk factors for pediatric acute respiratory distress syndrome (PARDS) after living donor liver transplantation (LDLT). However, studies of the relationship between HMGB1 and PARDS are lacking. We evaluated the link between anomalies of intraoperative serum HMGB1 and PARDS in pediatric LDLT recipients with biliary atresia during the first week after transplant. Methods Data for 210 pediatric patients with biliary atresia who underwent LDLT between January 2018 and December 2021 were reviewed retrospectively. The main measure was serum HMGB1 levels 30 min after reperfusion, while the outcome was early PARDS after LDLT. Data including pretransplant conditions, laboratory indexes, variables of intraoperation, clinical complications, and outcomes after LDLT were analyzed for each patient. Univariate analysis of PARDS and multivariate logistic regression analyses of serum HMGB1 levels at 30 min in the neohepatic phase in the presence of PARDS were conducted to examine the potential associations. Subgroup interaction analyses and linear relationships between intraoperative serum HMGB1 levels and PARDS were also performed. Results Among the participants, 55 had PARDS during 7 days after LDLT, including four in the first HMGB1 tertile (4.3–8.1 pg/mL), 18 in the second tertile (8.2–10.6 pg/mL), and 33 in the third tertile (10.6–18.8 pg/mL). The nonadjusted association between intraoperative HMGB1 levels and PARDS was positive (odds ratio 1.41, 95% confidence intervals 1.24–1.61, P < 0.0001). The association remained unchanged after adjustment for age, weight, pretransplant total bilirubin, albumin, graft cold ischemia time, and intraoperative blood loss volume (odds ratio 1.28, 95% confidence interval 1.10–1.49, P = 0.0017). After controlling for potential confounders, the association between intraoperative HMGB1 levels and PARDS remained positive, as well as in the subgroup analyses. Conclusions Serum HMGB1 levels at 30 min after reperfusion were positively associated with early PARDS among pediatric patients with biliary atresia who had undergone LDLT. Identifying such patients early may increase the efficacy of perioperative respiratory management.

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“…The released HMGB1 can further activate endothelial cells, leading to up-regulation of the cell adhesion molecules ICAM-1, VCAM-1, and E-selectin, and is involved in the cytokine secretion in cells ( 37 , 38 ). The released HMGB1 has also been found to induce early EC barrier disruption, with a potential molecular mechanism being activation of the RhoA/ROCK1 signaling pathway by HMGB1 via RAGE ( 39 ). These similarities between HMGB1 and histamine in the regulation of cell inflammatory and endothelial cell permeability indicate a possible relationship between them in the vascular system.…”

Section: Discussionmentioning

confidence: 99%

Histamine induced high mobility group box-1 release from vascular endothelial cells through H1 receptor

Gao

Liu

et al. 2022

Front. Immunol.

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BackgroundSystemic allergic reaction is characterized by vasodilation and vascular leakage, which causes a rapid, precipitous and sustained decrease in arterial blood pressure with a concomitant decrease of cardiac output. Histamine is a major mediator released by mast cells in allergic inflammation and response. It causes a cascade of inflammation and strongly increases vascular permeability within minutes through its four G-protein-coupled receptors (GPCRs) on endothelial cells. High mobility group box-1 (HMGB1), a nonhistone chromatin-binding nuclear protein, can be actively secreted into the extracellular space by endothelial cells. HMGB1 has been reported to exert pro-inflammatory effects on endothelial cells and to increase vascular endothelial permeability. However, the relationship between histamine and HMGB1-mediated signaling in vascular endothelial cells and the role of HMGB1 in anaphylactic-induced hypotension have never been studied.Methods and resultsEA.hy 926 cells were treated with different concentrations of histamine for the indicated periods. The results showed that histamine induced HMGB1 translocation and release from the endothelial cells in a concentration- and time-dependent manner. These effects of histamine were concentration-dependently inhibited by d-chlorpheniramine, a specific H1 receptor antagonist, but not by H2 or H3/4 receptor antagonists. Moreover, an H1-specific agonist, 2-pyridylethylamine, mimicked the effects of histamine, whereas an H2-receptor agonist, 4-methylhistamine, did not. Adrenaline and noradrenaline, which are commonly used in the clinical treatment of anaphylactic shock, also inhibited the histamine-induced HMGB1 translocation in endothelial cells. We therefore established a rat model of allergic shock by i.v. injection of compound 48/80, a potent histamine-releasing agent. The plasma HMGB1 levels in compound 48/80-injected rats were higher than those in controls. Moreover, the treatment with anti-HMGB1 antibody successfully facilitated the recovery from compound 48/80-induced hypotension.ConclusionHistamine induces HMGB1 release from vascular endothelial cells solely through H1 receptor stimulation. Anti-HMGB1 therapy may provide a novel treatment for life-threatening systemic anaphylaxis.

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Roles of RAGE/ROCK1 Pathway in HMGB1-Induced Early Changes in Barrier Permeability of Human Pulmonary Microvascular Endothelial Cell

Cited by 18 publications

References 37 publications

RAGE signaling regulates the progression of diabetic complications

RAGE signaling regulates the progression of diabetic complications

Association between serum HMGB1 elevation and early pediatric acute respiratory distress syndrome: a retrospective study of pediatric living donor liver transplant recipients with biliary atresia in China

Histamine induced high mobility group box-1 release from vascular endothelial cells through H1 receptor

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