The human lung cell line A549 does not develop adaptive protection against the DNA-damaging action of formaldehyde

2009 ◽  
pp. NA-NA
Author(s):  
Günter Speit ◽  
Simone Neuss ◽  
Oliver Schmid
Keyword(s):  
Cell Line ◽  
Human Lung ◽  
Adaptive Protection ◽  
Human Lung Cell Line ◽  
Lung Cell Line

P-317 Luteolin induce apoptosis in human lung cell line (A549) through activation of caspase 3 and p53

Lung Cancer ◽  
2003 ◽  
Vol 41 ◽  
pp. S172
Author(s):  
Te-Chun Hsia ◽  
Jing-Gung Chung ◽  
Hsueh-Fu Lu ◽  
Liang-Wen Hang ◽  
Wu-Huei Hsu ◽  
...  
Keyword(s):  
Cell Line ◽  
Caspase 3 ◽  
Human Lung ◽  
Human Lung Cell Line ◽  
Lung Cell Line

scholarly journals Implication of free radicals and glutathione in the mechanism of cadmium-induced expression of stress proteins in the A549 human lung cell-line

2000 ◽  
Vol 1495 (1) ◽  
pp. 4-13 ◽  
Author(s):  
Yolande Gaubin ◽  
Frédéric Vaissade ◽  
Françoise Croute ◽  
Bernadette Beau ◽  
Jean-Pierre Soleilhavoup ◽  
...  
Keyword(s):  
Free Radicals ◽  
Cell Line ◽  
Stress Proteins ◽  
Human Lung ◽  
Induced Expression ◽  
Human Lung Cell Line ◽  
Lung Cell Line

Combined toxic effect of airborne heavy metals on human lung cell line A549

2016 ◽  
Vol 40 (1) ◽  
pp. 271-282 ◽  
Author(s):  
Yeowool Choi ◽  
Kihong Park ◽  
Injeong Kim ◽  
Sang D. Kim
Keyword(s):  
Heavy Metals ◽  
Toxic Effect ◽  
Cell Line ◽  
Human Lung ◽  
Human Lung Cell Line ◽  
Lung Cell Line

ETA and ETB receptors cooperate in DNA synthesis via opposing regulations of cAMP in human lung cell line

1996 ◽  
Vol 271 (3) ◽  
pp. L366-L373
Author(s):  
M. Takimoto ◽  
K. Oda ◽  
T. Fruh ◽  
M. Takai ◽  
T. Okada ◽  
...  
Keyword(s):  
Dna Synthesis ◽  
Cell Line ◽  
Human Lung ◽  
Thymidine Incorporation ◽  
Selective Antagonists ◽  
Gi Protein ◽  
Camp Formation ◽  
Human Lung Cell Line ◽  
Lung Cell Line ◽  
Stimulation Of

We investigated the contribution of endothelin type A (ETA) and ETB receptors on ET-induced DNA synthesis in CCD-18Lu cells, a human lung cell line possessing both ETA and ETB (ETA/ETB ratio: 9:1). ET-1 (0.05-2 nM) potently induced [3H]thymidine incorporation by 2- to 14-fold over the basal level. An ETA-selective antagonist, FR139317, inhibited 0.2 nM ET-1-induced DNA synthesis dose dependently, showing complete inhibition at 1 microM. ET-3 was inactive up to 2 nM. In contrast, ETB-selective antagonists, 100 nM of BQ-788 or IRL 2500, partially (30-60%) inhibited 0.2 nM ET-1-induced DNA synthesis. Stimulation of either ETA or ETB evoked the increases in intracellular Ca2+ concentration ([Ca2+]i). ETB-mediated but not ET-1-induced [Ca2+]i increase was pertussis toxin (PTX) sensitive. Adenosine 3',5'-cyclic monophosphate (cAMP) formation via ETA was observed in PTX-treated cells, whereas the inhibition of isoproterenol-stimulated cAMP formation via ETB was observed in PTX-untreated cells. Like the ETB-selective antagonists, PTX treatment or dibutyryl cAMP partially (50-70%) inhibited ET-1-induced DNA synthesis. These data suggest that 1) ET-1 induces DNA synthesis predominantly through ETA, via PTX-insensitive G protein; 2) ETA-mediated cAMP formation inhibits DNA synthesis; and 3) stimulation of ETB coupling to Gi protein modulates ETA-mediated DNA synthesis by inhibiting cAMP formation.

scholarly journals Brilacidin, a COVID-19 Drug Candidate, Exhibits Potent In Vitro Antiviral Activity Against SARS-CoV-2

2020 ◽  
Author(s):  
Allison Bakovic ◽  
Kenneth Risner ◽  
Nishank Bhalla ◽  
Farhang Alem ◽  
Theresa L. Chang ◽  
...  
Keyword(s):  
Antiviral Activity ◽  
Cell Line ◽  
Small Molecule ◽  
Viral Entry ◽  
Human Lung ◽  
Drug Candidate ◽  
Human Lung Cell Line ◽  
Synthetic Small Molecule ◽  
Lung Cell Line

AbstractSummarySevere Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), the newly emergent causative agent of coronavirus disease-19 (COVID-19), has resulted in more than one million deaths worldwide since it was first detected in 2019. There is a critical global need for therapeutic intervention strategies that can be deployed to safely treat COVID-19 disease and reduce associated morbidity and mortality. Increasing evidence shows that both natural and synthetic antimicrobial peptides (AMPs), also referred to as Host Defense Proteins/Peptides (HDPs), can inhibit SARS-CoV-2, paving the way for the potential clinical use of these molecules as therapeutic options. In this manuscript, we describe the potent antiviral activity exerted by brilacidin—a de novo designed synthetic small molecule that captures the biological properties of HDPs—on SARS-CoV-2 in a human lung cell line (Calu-3) and a monkey cell line (Vero). These data suggest that SARS-CoV-2 inhibition in these cell culture models is primarily a result of the impact of brilacidin on viral entry and its disruption of viral integrity. Brilacidin has demonstrated synergistic antiviral activity when combined with remdesivir. Collectively, our data demonstrate that brilacidin exerts potent inhibition of SARS-CoV-2 and thus supports brilacidin as a promising COVID-19 drug candidate.HighlightsBrilacidin potently inhibits SARS-CoV-2 in an ACE2 positive human lung cell line.Brilacidin achieved a high Selectivity Index of 426 (CC50=241μM/IC50=0.565μM).Brilacidin’s main mechanism appears to disrupt viral integrity and impact viral entry.Brilacidin and remdesivir exhibit excellent synergistic activity against SARS-CoV-2.Significance StatementSARS-CoV-2, the emergent novel coronavirus, has led to the current global COVID-19 pandemic, characterized by extreme contagiousness and high mortality rates. There is an urgent need for effective therapeutic strategies to safely and effectively treat SARS-CoV-2 infection. We demonstrate that brilacidin, a synthetic small molecule with peptide-like properties, is capable of exerting potent in vitro antiviral activity against SARS-CoV-2, both as a standalone treatment and in combination with remdesivir, which is currently the only FDA-approved drug for the treatment of COVID-19.

Toxicity of tire debris extracts on human lung cell line A549

2005 ◽  
Vol 19 (7) ◽  
pp. 1001-1008 ◽  
Author(s):  
Maurizio Gualtieri ◽  
Laura Rigamonti ◽  
Valentina Galeotti ◽  
Marina Camatini
Keyword(s):  
Cell Line ◽  
Human Lung ◽  
Human Lung Cell Line ◽  
Lung Cell Line
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