CCCTC‐binding factor transcriptionally regulates Galectin‐7 and activates the JNK/STAT3 axis to aggravate bronchial epithelial cell injury

2021 ◽  
Author(s):  
Xinrong Sun ◽  
Wenna Shen ◽  
Zhaokun Li ◽  
Wanggang Zhang
Keyword(s):  
Epithelial Cell ◽  
Cell Injury ◽  
Bronchial Epithelial Cell ◽  
Bronchial Epithelial ◽  
Binding Factor ◽  
Epithelial Cell Injury

scholarly journals Ursolic Acid Inhibits Cigarette Smoke Extract-Induced Human Bronchial Epithelial Cell Injury and Prevents Development of Lung Cancer

Molecules ◽  
2012 ◽  
Vol 17 (8) ◽  
pp. 9104-9115 ◽  
Author(s):  
Wenbo Liu ◽  
Xiaobin Tan ◽  
Luan Shu ◽  
Hanyan Sun ◽  
Jie Song ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Epithelial Cell ◽  
Cigarette Smoke ◽  
Ursolic Acid ◽  
Cell Injury ◽  
Bronchial Epithelial Cell ◽  
Cigarette Smoke Extract ◽  
Human Bronchial Epithelial Cell ◽  
Bronchial Epithelial ◽  
Epithelial Cell Injury

scholarly journals MicroRNA-21 Mediates the Protective Effects of Mesenchymal Stem Cells Derived from iPSCs to Human Bronchial Epithelial Cell Injury Under Hypoxia

2018 ◽  
Vol 27 (3) ◽  
pp. 571-583 ◽  
Author(s):  
Cheng-Lin Li ◽  
Zhi-Bin Xu ◽  
Xing-Liang Fan ◽  
He-Xin Chen ◽  
Qiu-Ning Yu ◽  
...  
Keyword(s):  
Stem Cells ◽  
Mesenchymal Stem Cells ◽  
Epithelial Cell ◽  
Cell Injury ◽  
Bronchial Epithelial Cell ◽  
Human Bronchial Epithelial Cell ◽  
Epithelial Cell Line ◽  
Protective Effects ◽  
Bronchial Epithelial ◽  
Epithelial Cell Injury

Airway epithelial cell injury is a key triggering event to activate allergic airway inflammation, such as asthma. We previously reported that administration of mesenchymal stem cells (MSCs) significantly alleviated allergic inflammation in a mouse model of asthma, and the mmu-miR-21/ACVR2A axis may be involved. However, whether MSCs protect against bronchial epithelial cell injury induced by hypoxia, and the underlying mechanism, remain unknown. In our study, the human bronchial epithelial cell line BEAS-2B was induced to undergo apoptosis with a hypoxia mimic of cobalt chloride (CoCl2) damage. Treatment of MSCs derived from induced pluripotent stem cells (iPSCs) significantly decreased apoptosis of BEAS-2B cells. There was high miR-21 expression in injured BEAS-2B cells after MSC treatment. Transfection of the miR-21 mimic significantly decreased apoptosis of BEAS-2B, and transfection of a miR-21 inhibitor significantly increased apoptosis. More importantly, the protective effects of MSCs on injured BEAS-2B were reversed by transfection of the miR-21 inhibitor. Binding sites of human miR-21 were identified in the 3’UTR of human ACVR2A. We further determined that CoCl2 stimulation increased ACVR2A expression at both the mRNA and protein levels. Moreover, transfection of the miR-21 mimic further up-regulated ACVR2A expression induced by CoCl2, whereas transfection of the miR-21 inhibitor down-regulated ACVR2A expression. In addition, MSCs increased ACVR2A expression in BEAS-2B cells; however, this effect was reversed after transfection of the miR-21 inhibitor. Our data suggested that MSCs protect bronchial epithelial cells from hypoxic injury via miR-21, which may represent an important target. These findings suggest the potentially wide application of MSCs for epithelial cell injury during hypoxia.

microRNA-218 Inhibits Lipopolysaccharide-Induced Bronchial Epithelial Cell Injury by Targeting E2F2

2020 ◽  
Vol 10 (8) ◽  
pp. 1161-1169
Author(s):  
Min Gong ◽  
Zhongmei Mao ◽  
Jinni Chen ◽  
Xin Ye ◽  
Xiaobing Zhou
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Cell Viability ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Bronchial Epithelial Cell ◽  
Stress Injury ◽  
Bronchial Epithelial ◽  
Oxidative Stress Injury ◽  
And Oxidative Stress

Acute bronchopneumonia is a common hospitalization disease in children and serious acute bronchopneumonia will lead to death of children. MicroRNAs (miRNAs) have been thought to be related to inflammation in many diseases. The present study aimed to investigate the relation between miR218 and E2F2 and the effect of miR-218 overexpression and E2F2 inhibition on the improvement of inflammation in LPS-induced bronchial epithelial cell. BEAS-2B cells were induced by LPS for 0, 6, 12, 24 and 48 h which the cell viability was analyzed by CCK-8 assay. The expression of miR-218 in LPS-induced bronchial epithelial cell and cell transfection was detected by RT-qPCR analysis. The levels of TNF-α, IL-1α, and IL-6 in BEAS2B cells were detected using commercially-available ELISA kits. The levels of ROS, MDA, SOD and LDH were detected by ROS assay kit and oxidative stress assay kit. The cell apoptosis was analyzed by flow cytometry analysis and DAPI and hochest staining. As a result, miR-218 was decreased in LPS-induced bronchial epithelial cell. With the time of LPS treatment extends, the cell viability was decreased. Overexpression of miR-218 reduced the expression of inflammatory cytokines and oxidative stress injury in LPS-induced BEAS2B cells. Overexpression of miR-218 reduced apoptosis of LPS-induced BEAS2B cells. E2F2 was demonstrated be a target of miR-218 which miR-218 overexpression could inhibit the expression of E2F2. E2F2 inhibition could reverse the inflammatory and oxidative stress injury of LPS-induced BEAS2B cells caused by miR-218 inhibition. E2F2 inhibition could reverse the apoptosis of LPS-induced BEAS2B cells caused by miR-218 inhibition. In addition, E2F2 inhibition could reverse the expression of p-STAT1, cleaved-caspase3 and cleaved-caspase9 in LPS-induced BEAS2B cells caused by miR-218 inhibition. In conclusion, this study indicated that miR-218 overexpression and E2F2 inhibition can alleviate the inflammation in LPS-induced bronchial epithelial cell, thereby decreasing the oxidative stress and cell apoptosis.

scholarly journals Bronchial epithelial damage after a half-marathon in nonasthmatic amateur runners

2010 ◽  
Vol 298 (6) ◽  
pp. L857-L862 ◽  
Author(s):  
Laura Chimenti ◽  
Giuseppe Morici ◽  
Alessandra Paternò ◽  
Roberta Santagata ◽  
Anna Bonanno ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Injury ◽  
Bronchial Epithelial Cell ◽  
Induced Sputum ◽  
Intense Exercise ◽  
Bronchial Epithelial ◽  
Epithelial Damage ◽  
Peripheral Airways ◽  
Large Airways ◽  
Exercise In Humans

High neutrophil counts in induced sputum have been found in nonasthmatic amateur runners at rest and after a marathon, but the pathogenesis of airway neutrophilia in athletes is still poorly understood. Bronchial epithelial damage may occur during intense exercise, as suggested by investigations conducted in endurance-trained mice and competitive human athletes studied under resting conditions. To gain further information on airway changes acutely induced by exercise, airway cell composition, apoptosis, IL-8 concentration in induced sputum, and serum CC-16 level were measured in 15 male amateur runners at rest (baseline) and shortly after a half-marathon. Different from results obtained after a marathon, neutrophil absolute counts were unchanged, whereas bronchial epithelial cell absolute counts and their apoptosis increased significantly ( P < 0.01). IL-8 in induced sputum supernatants almost doubled postrace compared with baseline ( P < 0.01) and correlated positively with bronchial epithelial cell absolute counts ( R2 = 0.373, P < 0.01). Serum CC-16 significantly increased after all races ( P < 0.01). These data show mild bronchial epithelial cell injury acutely induced by intense endurance exercise in humans, extending to large airways the data obtained in peripheral airways of endurance-trained mice. Therefore, neutrophil influx into the airways of athletes may be secondary to bronchial epithelial damage associated with intense exercise.

scholarly journals Comparison of host endothelial, epithelial and inflammatory response in ICU patients with and without COVID-19: a prospective observational cohort study

Critical Care ◽  
2021 ◽  
Vol 25 (1) ◽  
Author(s):  
Pavan K. Bhatraju ◽  
Eric D. Morrell ◽  
Leila Zelnick ◽  
Neha A. Sathe ◽  
Xin-Ya Chai ◽  
...  
Keyword(s):  
Endothelial Dysfunction ◽  
Epithelial Cell ◽  
Acute Phase ◽  
Cell Injury ◽  
Acute Phase Proteins ◽  
Invasive Mechanical Ventilation ◽  
Icu Patients ◽  
Icu Admission ◽  
Amyloid A ◽  
Epithelial Cell Injury

Abstract Background Analyses of blood biomarkers involved in the host response to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) viral infection can reveal distinct biological pathways and inform development and testing of therapeutics for COVID-19. Our objective was to evaluate host endothelial, epithelial and inflammatory biomarkers in COVID-19. Methods We prospectively enrolled 171 ICU patients, including 78 (46%) patients positive and 93 (54%) negative for SARS-CoV-2 infection from April to September, 2020. We compared 22 plasma biomarkers in blood collected within 24 h and 3 days after ICU admission. Results In critically ill COVID-19 and non-COVID-19 patients, the most common ICU admission diagnoses were respiratory failure or pneumonia, followed by sepsis and other diagnoses. Similar proportions of patients in both groups received invasive mechanical ventilation at the time of study enrollment. COVID-19 and non-COVID-19 patients had similar rates of acute respiratory distress syndrome, severe acute kidney injury, and in-hospital mortality. While concentrations of interleukin 6 and 8 were not different between groups, markers of epithelial cell injury (soluble receptor for advanced glycation end products, sRAGE) and acute phase proteins (serum amyloid A, SAA) were significantly higher in COVID-19 compared to non-COVID-19, adjusting for demographics and APACHE III scores. In contrast, angiopoietin 2:1 (Ang-2:1 ratio) and soluble tumor necrosis factor receptor 1 (sTNFR-1), markers of endothelial dysfunction and inflammation, were significantly lower in COVID-19 (p < 0.002). Ang-2:1 ratio and SAA were associated with mortality only in non-COVID-19 patients. Conclusions These studies demonstrate that, unlike other well-studied causes of critical illness, endothelial dysfunction may not be characteristic of severe COVID-19 early after ICU admission. Pathways resulting in elaboration of acute phase proteins and inducing epithelial cell injury may be promising targets for therapeutics in COVID-19.

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