scholarly journals Gadd45α activity is the principal effector of Shigella mitochondria-dependent epithelial cell death in vitro and ex vivo

2011 ◽  
Vol 2 (2) ◽  
pp. e122-e122 ◽  
Author(s):  
L Lembo-Fazio ◽  
G Nigro ◽  
G Noël ◽  
G Rossi ◽  
F Chiara ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Ex Vivo ◽  
Epithelial Cell Death

Protective effect of IL-6 on alveolar epithelial cell death induced by hydrogen peroxide

2005 ◽  
Vol 288 (2) ◽  
pp. L342-L349 ◽  
Author(s):  
Hiroshi Kida ◽  
Mitsuhiro Yoshida ◽  
Shigenori Hoshino ◽  
Koji Inoue ◽  
Yukihiro Yano ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Epithelial Cell ◽  
Epithelial Cells ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial Cells ◽  
Lung Fibroblasts ◽  
Alveolar Epithelial ◽  
Epithelial Cell Death

The goal of this study was to examine whether IL-6 could directly protect lung resident cells, especially alveolar epithelial cells, from reactive oxygen species (ROS)-induced cell death. ROS induced IL-6 gene expression in organotypic lung slices of wild-type (WT) mice. ROS also induced IL-6 gene expression in mouse primary lung fibroblasts, dose dependently. The organotypic lung slices of WT were more resistant to ROS-induced DNA fragmentation than those of IL-6-deficient (IL-6−/−) mice. WT resistance against ROS was abrogated by treatment with anti-IL-6 antibody. TdT-mediated dUTP nick end labeling stain and electron microscopy revealed that DNA fragmented cells in the IL-6−/− slice included alveolar epithelial cells and endothelial cells. In vitro studies demonstrated that IL-6 reduced ROS-induced A549 alveolar epithelial cell death. Together, these data suggest that IL-6 played an antioxidant role in the lung by protecting lung resident cells, especially alveolar epithelial cells, from ROS-induced cell death.

scholarly journals Dexmedetomidine Attenuates Bilirubin-Induced Lung Alveolar Epithelial Cell Death In Vitro and In Vivo*

2015 ◽  
Vol 43 (9) ◽  
pp. e356-e368 ◽  
Author(s):  
Jian Cui ◽  
Hailin Zhao ◽  
Bin Yi ◽  
Jing Zeng ◽  
Kaizhi Lu ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Alveolar Epithelial Cell ◽  
Alveolar Epithelial ◽  
Epithelial Cell Death

scholarly journals Platelets inhibit apoptotic lung epithelial cell death and protect mice against infection-induced lung injury

2019 ◽  
Vol 3 (3) ◽  
pp. 432-445 ◽  
Author(s):  
William Bain ◽  
Tolani Olonisakin ◽  
Minting Yu ◽  
Yanyan Qu ◽  
Mei Hulver ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Lung Injury ◽  
Lung Epithelial Cell ◽  
Barrier Disruption ◽  
Lung Epithelial ◽  
Epithelial Cell Death ◽  
Alveolar Capillary

Abstract Thrombocytopenia is associated with worse outcomes in patients with acute respiratory distress syndrome, which is most commonly caused by infection and marked by alveolar–capillary barrier disruption. However, the mechanisms by which platelets protect the lung alveolar–capillary barrier during infectious injury remain unclear. We found that natively thrombocytopenic Mpl−/− mice deficient in the thrombopoietin receptor sustain severe lung injury marked by alveolar barrier disruption and hemorrhagic pneumonia with early mortality following acute intrapulmonary Pseudomonas aeruginosa (PA) infection; barrier disruption was attenuated by platelet reconstitution. Although PA infection was associated with a brisk neutrophil influx, depletion of airspace neutrophils failed to substantially mitigate PA-triggered alveolar barrier disruption in Mpl−/− mice. Rather, PA cell-free supernatant was sufficient to induce lung epithelial cell apoptosis in vitro and in vivo and alveolar barrier disruption in both platelet-depleted mice and Mpl−/− mice in vivo. Cell-free supernatant from PA with genetic deletion of the type 2 secretion system, but not the type 3 secretion system, mitigated lung epithelial cell death in vitro and lung injury in Mpl−/− mice. Moreover, platelet releasates reduced poly (ADP ribose) polymerase cleavage and lung injury in Mpl−/− mice, and boiling of platelet releasates, but not apyrase treatment, abrogated PA supernatant–induced lung epithelial cell cytotoxicity in vitro. These findings indicate that while neutrophil airspace influx does not potentiate infectious lung injury in the thrombocytopenic host, platelets and their factors protect against severe pulmonary complications from pathogen-secreted virulence factors that promote host cell death even in the absence of overt infection.

scholarly journals Extracellular vesicle-cargo miR-185-5p reflects type II alveolar cell death after oxidative stress

2020 ◽  
Vol 6 (1) ◽  
Author(s):  
Jonathan M. Carnino ◽  
Heedoo Lee ◽  
Xue He ◽  
Michael Groot ◽  
Yang Jin
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Alveolar Epithelial Cell ◽  
Extracellular Vesicle ◽  
Alveolar Type ◽  
Type I ◽  
Type Ii ◽  
Alveolar Cells ◽  
Epithelial Cell Death

Abstract Acute respiratory distress syndrome (ARDS) is a devastating syndrome responsible for significant morbidity and mortality. Diffuse alveolar epithelial cell death, including but not limited to apoptosis and necroptosis, is one of the hallmarks of ARDS. Currently, no detectable markers can reflect this feature of ARDS. Hyperoxia-induced lung injury is a well-established murine model that mimics human ARDS. We found that hyperoxia and its derivative, reactive oxygen species (ROS), upregulate miR-185-5p, but not miR-185-3p, in alveolar cells. This observation is particularly more significant in alveolar type II (ATII) than alveolar type I (ATI) cells. Functionally, miR-185-5p promotes expression and activation of both receptor-interacting kinase I (RIPK1) and receptor-interacting kinase III (RIPK3), leading to phosphorylation of mixed lineage kinase domain-like (MLKL) and necroptosis. MiR-185-5p regulates this process probably via suppressing FADD and caspase-8 which are both necroptosis inhibitors. Furthermore, miR-185-5p also promotes intrinsic apoptosis, reflected by enhancing caspase-3/7 and 9 activity. Importantly, extracellular vesicle (EV)-containing miR-185-5p, but not free miR-185-5p, is detectable and significantly elevated after hyperoxia-induced cell death, both in vitro and in vivo. Collectively, hyperoxia-induced miR-185-5p regulates both necroptosis and apoptosis in ATII cells. The extracellular level of EV-cargo miR-185-5p is elevated in the setting of profound epithelial cell death.

scholarly journals Inhibition of epithelial cell death in the secondary palate in vitro by alteration of lysosome function.

1978 ◽  
Vol 26 (12) ◽  
pp. 1109-1114 ◽  
Author(s):  
R M Greene ◽  
R M Pratt
Keyword(s):  
Cell Death ◽  
Acid Phosphatase ◽  
Epithelial Cell ◽  
Lysosomal Enzymes ◽  
Developmental Age ◽  
Secondary Palate ◽  
Epithelial Cell Death ◽  
Histochemical Examination

The secondary palate in vivo and in vitro exhibits selective cell death at its medialedge epithelium (MEE) at a precise developmental age. This epithelial degeneration is mediated, in part, by MEE lysosomes. Previous studies in vitro (27) showed that the glutamine analogue, diazo-oxo-norleucine (DON), prevented MEE cell death by inhibiting glucosamine synthesis and thereby the glycosylation of proteins without affecting either the synthesis or activity of palatal lysosomal enzymes. In the present study, histochemical examination of MEE from DON treated day-15 rat palates demonstrated that acid phosphatase activity was restricted to Golgi saccules and associated vesicles as well as to lysosomes. Control MEE had reaction product in these structures and distributed diffusely throughout the cytoplasm of degenerating cells. DON treatment therefore appears to alter the intracellular distribution of lysosomal enzymes. Since DON treatment appears to have prevented MEE cell death by inhibiting glycosylation of proteins, glycosylation of lysosomal membranes or lysosomal enzymes may be essential for its role in programmed cell death.

scholarly journals Nitric Oxide Is an Important Mediator of Renal Tubular Epithelial Cell Death in Vitro and in Murine Experimental Hydronephrosis

2006 ◽  
Vol 169 (2) ◽  
pp. 388-399 ◽  
Author(s):  
Tiina Kipari ◽  
Jean-Francois Cailhier ◽  
David Ferenbach ◽  
Simon Watson ◽  
Kris Houlberg ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Cell Death ◽  
Epithelial Cell ◽  
Tubular Epithelial Cell ◽  
Renal Tubular Epithelial Cell ◽  
Important Mediator ◽  
Renal Tubular ◽  
Epithelial Cell Death ◽  
Experimental Hydronephrosis
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