scholarly journals SIRT1 Regulates the Human Alveolar Epithelial A549 Cell Apoptosis Induced byPseudomonas AeruginosaLipopolysaccharide

2013 ◽  
Vol 31 (1) ◽  
pp. 92-101 ◽  
Author(s):  
Xiaoli Liu ◽  
Kuiqing Shao ◽  
Tieying Sun
Keyword(s):  
A549 Cell ◽  
Cell Apoptosis ◽  
Alveolar Epithelial

Ghrelin ameliorates the human alveolar epithelial A549 cell apoptosis induced by lipopolysaccharide

2016 ◽  
Vol 474 (1) ◽  
pp. 83-90 ◽  
Author(s):  
Chunrong Huang ◽  
Haichong Zheng ◽  
Wanmei He ◽  
Guifang Lu ◽  
Xia Li ◽  
...  
Keyword(s):  
A549 Cell ◽  
Cell Apoptosis ◽  
Alveolar Epithelial

scholarly journals Retraction: FOXC1 silencing promotes A549 cell apoptosis through inhibiting the PI3K/AKT/hedgehog/Gli2 signaling pathway

RSC Advances ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 4572-4572
Author(s):  
Laura Fisher
Keyword(s):  
Signaling Pathway ◽  
A549 Cell ◽  
Cell Apoptosis

Retraction of ‘FOXC1 silencing promotes A549 cell apoptosis through inhibiting the PI3K/AKT/hedgehog/Gli2 signaling pathway’ by Pei Wang et al., RSC Adv., 2018, 8, 33786–33793, DOI: 10.1039/C8RA06041J.

scholarly journals Mir-204 Regulates LPS-Induced A549 Cell Damage by Targeting FOXK2

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Shufen Li ◽  
Lifen Zhao ◽  
Xujiong Li ◽  
Gaiping Shang ◽  
Lijing Gao ◽  
...  
Keyword(s):  
A549 Cell ◽  
Cell Apoptosis ◽  
Cell Injury ◽  
Cell Damage ◽  
A549 Cells ◽  
Inflammatory Factors ◽  
Luciferase Reporter ◽  
Luciferase Reporter Gene ◽  
Downstream Target ◽  
Apoptosis Related Protein

Objective. To assess whether miR-204 and HA affect A549 cell injury induced by lipopolysaccharide. Material and Methods. A549 cells were treated with hirsutanol A, and cell damage was induced by LPS followed by analysis of cell proliferation by CCK-8, cell apoptosis by flow cytometry, apoptosis-related protein expression by western blot, downstream target of miR-20 by dual-luciferase reporter gene, and inflammatory factors by ELISA and PCR. Results. LPS can significantly inhibit the viability of A549 cells, induce cell apoptosis, and promote the release of IL-6, IL-1β, and TNF-α, while HA pretreatment can target FOXK2 by upregulating miR-204 levels, thereby alleviating apoptosis and promoting cell viability and at the same time inhibiting the release of inflammatory factors by inhibiting the activation of NF-κB. Conclusions. miR-204 participates in the protection of HA acute lung injury by targeting FOXK2.

Study on the antitumor activity and mechanism of novel targeted nanodrugs based on miRNA in cervical cancer

2020 ◽  
Vol 10 (8) ◽  
pp. 1218-1223
Author(s):  
Xinping Chen ◽  
Zhichao Ma ◽  
Juan Zhu ◽  
Weihua Xu ◽  
Junjie Hu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Flow Cytometry ◽  
Antitumor Activity ◽  
A549 Cell ◽  
Cell Apoptosis ◽  
Caspase 3 ◽  
A549 Cells ◽  
Dependent Manner ◽  
Double Staining ◽  
Dose Dependent

The aim of this study was to investigate the effect of different concentrations of novel targeted nanodrugs based on miRNA on the antitumor activity and mechanism in cervical carcinoma A549 cells. The MTT method was used to determine the effect of different concentrations of novel targeted nanodrugs based on miRNA on A549 cell proliferation, and annexin V FITC/PI double staining flow cytometry was performed to analyze the effect of these nanodrugs on A549 cell apoptosis. Western blotting was performed to observe the effect of these nanodrugs on the expression of Bax, Bcl-2, and caspase-3-related genes involved in A549 cell apoptosis. Compared with the control group, the novel targeted nanodrugs based on miRNA significantly inhibited the proliferation of A549 cells in a time- and dose-dependent manner. Results of double staining flow cytometry demonstrated that these nanodrugs could increase the apoptotic rate of A549 cells in a dose-dependent manner 48 h later. Western blotting revealed that these nanodrugs could upregulate the expression of Bax and caspase3 genes and downregulate the expression of Bcl-2 gene. Nanodrugs display an obvious antitumor activity in vitro, and the underlying mechanism may be associated with the upregulation of Bax and caspase-3 gene expression and the downregulation of Bcl-2 gene expression.

Hyperoxia-induced apoptosis and Fas/FasL expression in lung epithelial cells

2005 ◽  
Vol 289 (4) ◽  
pp. L647-L659 ◽  
Author(s):  
Monique E. De Paepe ◽  
Quanfu Mao ◽  
Yvonne Chao ◽  
Jessica L. Powell ◽  
Lewis P. Rubin ◽  
...  
Keyword(s):  
Cell Death ◽  
Epithelial Cells ◽  
Protein Expression ◽  
Cell Apoptosis ◽  
Receptor Activation ◽  
Type Ii ◽  
Fasl Expression ◽  
Alveolar Epithelial ◽  
Type Ii Cell ◽  
Induced Apoptosis

Alveolar epithelial apoptosis is an important feature of hyperoxia-induced lung injury in vivo and has been described in the early stages of bronchopulmonary dysplasia (chronic lung disease of preterm newborn). Molecular regulation of hyperoxia-induced alveolar epithelial cell death remains incompletely understood. In view of functional involvement of Fas/FasL system in physiological postcanalicular type II cell apoptosis, we speculated this system may also be a critical regulator of hyperoxia-induced apoptosis. The aim of this study was to investigate the effects of hyperoxia on apoptosis and apoptotic gene expression in alveolar epithelial cells. Apoptosis was studied by TUNEL, electron microscopy, DNA size analysis, and caspase assays. Fas/FasL expression was determined by Western blot analysis and RPA. We determined that in MLE-12 cells exposed to hyperoxia, caspase-mediated apoptosis was the first morphologically and biochemically recognizable mode of cell death, followed by necrosis of residual adherent cells. The apoptotic stage was associated with a threefold upregulation of Fas mRNA and protein expression and increased susceptibility to direct Fas receptor activation, concomitant with a threefold increase of FasL protein levels. Fas gene silencing by siRNAs significantly reduced hyperoxia-induced apoptosis. In murine fetal type II cells, hyperoxia similarly induced markedly increased Fas/FasL protein expression, confirming validity of results obtained in transformed MLE-12 cells. Our findings implicate the Fas/FasL system as an important regulator of hyperoxia-induced type II cell apoptosis. Elucidation of regulation of hyperoxia-induced lung apoptosis may lead to alternative therapeutic strategies for perinatal or adult pulmonary diseases characterized by dysregulated type II cell apoptosis.

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