Cigarette Smoke-Induced Oxidative Stress and Autophagy in Human Alveolar Epithelial Cell Line (A549 Cells)

2019 ◽  
pp. 63-69 ◽  
Author(s):  
P. Szoka ◽  
J. Lachowicz ◽  
M. Cwiklińska ◽  
A. Lukaszewicz ◽  
A. Rybak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Cell Line ◽  
Cigarette Smoke ◽  
Alveolar Epithelial Cell ◽  
A549 Cells ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell

Cytotoxicity, oxidative stress and genotoxicity induced by glass fibers on human alveolar epithelial cell line A549

2015 ◽  
Vol 29 (3) ◽  
pp. 551-557 ◽  
Author(s):  
Venerando Rapisarda ◽  
Carla Loreto ◽  
Caterina Ledda ◽  
Giuseppe Musumeci ◽  
Massimo Bracci ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Glass Fibers ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell

Effect of Steroids on the Synthesis of Complement C3 in a Human Alveolar Epithelial Cell Line

1993 ◽  
Vol 19 (5) ◽  
pp. 603-616 ◽  
Author(s):  
Terence L. Zach ◽  
Vicki A. Herrman ◽  
Laura D. Hill ◽  
M. Patricia Leuschen
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Complement C3 ◽  
Epithelial Cell Line ◽  
Alveolar Epithelial ◽  
Human Alveolar Epithelial Cell

scholarly journals Transcriptional and Proteomic Characterization of Telomere-Induced Senescence in a Human Alveolar Epithelial Cell Line

2021 ◽  
Vol 8 ◽  
Author(s):  
Daniel I. Sullivan ◽  
Mao Jiang ◽  
Angela M. Hinchie ◽  
Mark G. Roth ◽  
Harinath Bahudhanapati ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Line ◽  
Alveolar Epithelial Cell ◽  
Epithelial Cell Line ◽  
Telomere Dysfunction ◽  
Alveolar Epithelial ◽  
Novel Proteins ◽  
Human Alveolar Epithelial Cell ◽  
Species Specific

Cellular senescence due to telomere dysfunction has been hypothesized to play a role in age-associated diseases including idiopathic pulmonary fibrosis (IPF). It has been postulated that paracrine mediators originating from senescent alveolar epithelia signal to surrounding mesenchymal cells and contribute to disease pathogenesis. However, murine models of telomere-induced alveolar epithelial senescence fail to display the canonical senescence-associated secretory phenotype (SASP) that is observed in senescent human cells. In an effort to understand human-specific responses to telomere dysfunction, we modeled telomere dysfunction-induced senescence in a human alveolar epithelial cell line. We hypothesized that this system would enable us to probe for differences in transcriptional and proteomic senescence pathways in vitro and to identify novel secreted protein (secretome) changes that potentially contribute to the pathogenesis of IPF. Following induction of telomere dysfunction, a robust senescence phenotype was observed. RNA-seq analysis of the senescent cells revealed the SASP and comparisons to previous murine data highlighted differences in response to telomere dysfunction. We conducted a proteomic analysis of the senescent cells using a novel biotin ligase capable of labeling secreted proteins. Candidate biomarkers selected from our transcriptional and secretome data were then evaluated in IPF and control patient plasma. Four novel proteins were found to be differentially expressed between the patient groups: stanniocalcin-1, contactin-1, tenascin C, and total inhibin. Our data show that human telomere-induced, alveolar epithelial senescence results in a transcriptional SASP that is distinct from that seen in analogous murine cells. Our findings suggest that studies in animal models should be carefully validated given the possibility of species-specific responses to telomere dysfunction. We also describe a pragmatic approach for the study of the consequences of telomere-induced alveolar epithelial cell senescence in humans.

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