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 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.

Alveolar epithelial cell death adjacent to underlying myofibroblasts in advanced fibrotic human lung

1998 ◽  
Vol 275 (6) ◽  
pp. L1192-L1199 ◽  
Author(s):  
Bruce D. Uhal ◽  
Iravati Joshi ◽  
W. Frank Hughes ◽  
Carlos Ramos ◽  
Annie Pardo ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Human Lung ◽  
Alveolar Epithelial Cell ◽  
Cell Loss ◽  
Alveolar Epithelial ◽  
Picrosirius Red ◽  
Epithelial Cell Death

Earlier work from this laboratory showed that abnormal fibroblast phenotypes isolated from fibrotic human lung produce factor(s) capable of inducing apoptosis and necrosis of alveolar epithelial cells in vitro [B. D. Uhal, I. Joshi, A. True, S. Mundle, A. Raza, A. Pardo, and M. Selman. Am. J. Physiol. 269 ( Lung Cell. Mol. Physiol. 13): L819–L828, 1995]. To determine whether epithelial cell death is associated with proximity to abnormal fibroblasts in vivo, the spatial distribution of epithelial cell loss, DNA fragmentation, and myofibroblasts was examined in the same tissue specimens used previously for fibroblast isolation. Paraffin sections of normal and fibrotic human lung were subjected to in situ end labeling (ISEL) of fragmented DNA and simultaneous immunolabeling of α-smooth muscle actin (α-SMA); replicate samples were subjected to electron microscopy and detection of collagens by the picrosirius red technique. Normal human lung exhibited very little labeling except for positive α-SMA immunoreactivity of smooth muscle surrounding bronchi and vessels. In contrast, fibrotic human lung exhibited moderate to heavy ISEL of interstitial, cuboidal epithelial, and free alveolar cells. ISEL of the alveolar epithelium was not distributed uniformly but was most intense immediately adjacent to underlying foci of α-SMA-positive fibroblast-like interstitial cells. Both electron microscopy and picrosirius red confirmed epithelial cell apoptosis, necrosis, and cell loss adjacent to foci of collagen accumulation surrounding fibroblast-like cells. These results demonstrate that the cuboidal epithelium of the fibrotic lung contains dying as well as proliferating cells and support the hypothesis that alveolar epithelial cell death is induced by abnormal lung fibroblasts in vivo as it is in vitro.

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 TLR3, TRIF, and Caspase 8 Determine Double-Stranded RNA-Induced Epithelial Cell Death and Survival In Vivo

2012 ◽  
Vol 190 (1) ◽  
pp. 418-427 ◽  
Author(s):  
Christopher S. McAllister ◽  
Omar Lakhdari ◽  
Guillaume Pineton de Chambrun ◽  
Mélanie G. Gareau ◽  
Alexis Broquet ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cell ◽  
Caspase 8 ◽  
Double Stranded Rna ◽  
Epithelial Cell Death

scholarly journals Fusobacterium nucleatum Promotes the Development of Ulcerative Colitis by Inducing the Autophagic Cell Death of Intestinal Epithelial

2020 ◽  
Vol 10 ◽  
Author(s):  
Wenhao Su ◽  
Yongyu Chen ◽  
Pan Cao ◽  
Yan Chen ◽  
Yuanmei Guo ◽  
...  
Keyword(s):  
Ulcerative Colitis ◽  
Cell Death ◽  
Epithelial Cell ◽  
Clinical Characteristics ◽  
Intestinal Epithelial Cell ◽  
Fusobacterium Nucleatum ◽  
Autophagic Cell Death ◽  
Intestinal Epithelial

There is a growing body of evidence which suggests that intestinal microbiota, especially Fusobacterium nucleatum (F. nucleatum), are associated with intestinal immune disease such as ulcerative colitis (UC). The mechanism by which F. nucleatum promotes intestinal epithelial cell (IEC) death remained undefined. Here, we investigated the potential mechanisms about how F. nucleatum aggravates IEC death in UC. We first detected the abundance of F. nucleatum in UC tissues and analyzed its relationship with the clinical characteristics of UC. Next, we explored whether F. nucleatum promotes intestinal epithelial cell death in vitro and in vivo. Furthermore, we extracted lipopolysaccharide (LPS) of the F. nucleatum and examined whether F. nucleatum exacerbates UC via LPS. Our results indicated that F. nucleatum was abundant in UC tissues and was correlated with clinical characteristics. In addition, we demonstrated that F. nucleatum and its LPS aggravated IEC death by promoted IEC autophagy. Furthermore, autophagy inhibitors, chloroquine (CQ), 3-methyladenine (3-MA) or Atg5 silencing prevented IEC death mediated by F. nucleatum, which suggests F. nucleatum may contribute to UC by activating autophagic cell death. All our results uncover a vital role of F. nucleatum in autophagic cell death and UC, giving rise to a new sight for UC therapy by inhibiting excessive IEC autophagy and autophagic cell death.

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