scholarly journals Pulmonary Endothelial Cell Apoptosis in Emphysema and Acute Lung Injury

2017 ◽  
pp. 63-86 ◽  
Author(s):  
Eboni Chambers ◽  
Sharon Rounds ◽  
Qing Lu
Keyword(s):  
Acute Lung Injury ◽  
Endothelial Cell ◽  
Lung Injury ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis

Endothelial Cell Apoptosis in Lipopolysaccharide–Induced Lung Injury in Mice

1998 ◽  
Vol 117 (3) ◽  
pp. 202-208 ◽  
Author(s):  
Masaki Fujita ◽  
Kazuyoshi Kuwano ◽  
Ritsuko Kunitake ◽  
Naoki Hagimoto ◽  
Hiroyuki Miyazaki ◽  
...  
Keyword(s):  
Endothelial Cell ◽  
Lung Injury ◽  
Cell Apoptosis ◽  
Endothelial Cell Apoptosis

scholarly journals Fatty Acid Oxidation Protects against Hyperoxia-induced Endothelial Cell Apoptosis and Lung Injury in Neonatal Mice

2019 ◽  
Vol 60 (6) ◽  
pp. 667-677 ◽  
Author(s):  
Hongwei Yao ◽  
Jiannan Gong ◽  
Abigail L. Peterson ◽  
Xuexin Lu ◽  
Peng Zhang ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Endothelial Cell ◽  
Lung Injury ◽  
Fatty Acid Oxidation ◽  
Cell Apoptosis ◽  
Acid Oxidation ◽  
Endothelial Cell Apoptosis ◽  
Neonatal Mice

scholarly journals Uric acid promotes oxidative stress and enhances vascular endothelial cell apoptosis in rats with middle cerebral artery occlusion

2018 ◽  
Vol 38 (3) ◽  
Author(s):  
Chengfu Song ◽  
Xiangdong Zhao
Keyword(s):  
Oxidative Stress ◽  
Uric Acid ◽  
Endothelial Cell ◽  
Cell Apoptosis ◽  
Vascular Endothelial Cell ◽  
Artery Occlusion ◽  
Vascular Endothelial ◽  
Endothelial Cell Apoptosis ◽  
Related Factors ◽  
Cerebral Artery Occlusion

In patients with cerebral infarction (CI), elevated serum uric acid (UA) level may exacerbate the occurrence and development of carotid atherosclerosis (AS). Our study intended to explore the underlying mechanism. We enrolled 86 patients with CI, and divided them into four groups: Non-AS, AS-mild, AS-moderate, and AS-severe groups; the levels of UA and oxidative stress-related factors in serum were detected. The middle cerebral artery occlusion (MCAO) model was used to stimulate CI in rats, and different doses of UA were administrated. The levels of oxidative stress-related factors in serum were detected. Hematoxylin & eosin (H&E) staining was used to observe the morphological alterations, and the apoptotic cell death detection kit was used to detect apoptotic cells. Increased UA concentration and enhanced oxidative stress were found in AS patients. H&E staining results showed that UA treatment exacerbated morphological damage in rats with MCAO, promoted oxidative stress, and enhanced vascular endothelial cell apoptosis in rats with MCAO.

Maternal Anti-HPA-1a Antibodies Increase Endothelial Cell Apoptosis and Permeability

2021 ◽  
pp. 1-9
Author(s):  
Rima Dardik ◽  
Ophira Salomon
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Intracranial Hemorrhage ◽  
Cell Apoptosis ◽  
Endothelial Damage ◽  
Αvβ3 Integrin ◽  
Endothelial Cell Apoptosis ◽  
Vascular Beds ◽  
Alloimmune Thrombocytopenia

Intracranial hemorrhage (ICH) associated with fetal/neonatal alloimmune thrombocytopenia (FNAIT) is attributed mainly to endothelial damage caused by binding of maternal anti-HPA-1a antibodies to the αvβ3 integrin on endothelial cells (ECs). We examined the effect of anti-HPA-1a antibodies on EC function using 2 EC lines from different vascular beds, HMVEC of dermal origin and hCMEC/D3 of cerebral origin. Anti-HPA-1a sera significantly increased apoptosis in both HMVEC and hCMEC/D3 cells and permeability in hCMEC/D3 cells only. This increase in both apoptosis and permeability was significantly inhibited by a monoclonal anti-β3 antibody (SZ21) binding to the HPA-1a epitope. Our results indicate that (1) maternal anti-HPA-1a antibodies impair EC function by increasing apoptosis and permeability and (2) ECs from different vascular beds vary in their susceptibility to pathological effects elicited by maternal anti-HPA-1a antibodies on EC permeability. Examination of maternal anti-HPA-1a antibodies for their effect on EC permeability may predict potential ICH associated with FNAIT.

scholarly journals Long non-coding RNA OIP5-AS1 aggravates acute lung injury by promoting inflammation and cell apoptosis via regulating the miR-26a-5p/TLR4 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Qingsong Sun ◽  
Man Luo ◽  
Zhiwei Gao ◽  
Xiang Han ◽  
Weiqin Wu ◽  
...  
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Inflammatory Response ◽  
Cell Apoptosis ◽  
Quantitative Polymerase Chain Reaction ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Interacting Protein ◽  
Wide Range

Abstract Background Acute lung injury (ALI) is a pulmonary disorder that leads to acute respiration failure and thereby results in a high mortality worldwide. Increasing studies have indicated that toll-like receptor 4 (TLR4) is a promoter in ALI, and we aimed to explore the underlying upstream mechanism of TLR4 in ALI. Methods We used lipopolysaccharide (LPS) to induce an acute inflammatory response in vitro model and a murine mouse model. A wide range of experiments including reverse transcription quantitative polymerase chain reaction, western blot, enzyme linked immunosorbent assay, flow cytometry, hematoxylin–eosin staining, RNA immunoprecipitation, luciferase activity and caspase-3 activity detection assays were conducted to figure out the expression status, specific role and potential upstream mechanism of TLR4 in ALI. Result TLR4 expression was upregulated in ALI mice and LPS-treated primary bronchial/tracheal epithelial cells. Moreover, miR-26a-5p was confirmed to target TLR4 according to results of luciferase reporter assay. In addition, miR-26a-5p overexpression decreased the contents of proinflammatory factors and inhibited cell apoptosis, while upregulation of TLR4 reversed these effects of miR-26a-5p mimics, implying that miR-26a-5p alleviated ALI by regulating TLR4. Afterwards, OPA interacting protein 5 antisense RNA 1 (OIP5-AS1) was identified to bind with miR-26a-5p. Functionally, OIP5-AS1 upregulation promoted the inflammation and miR-26a-5p overexpression counteracted the influence of OIP5-AS1 upregulation on cell inflammatory response and apoptosis. Conclusion OIP5-AS1 promotes ALI by regulating the miR-26a-5p/TLR4 axis in ALI mice and LPS-treated cells, which indicates a promising insight into diagnostics and therapeutics in ALI.

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