Short-Term versus Long-Term Culture of A549 Cells for Evaluating the Effects of Lipopolysaccharide on Oxidative Stress, Surfactant Proteins and Cathelicidin LL-37

Nová, Zuzana; Škovierová, Henrieta; Strnádel, Ján; Halašová, Erika; Čalkovská, Andrea

doi:10.3390/ijms21031148

Cited by 19 publications

(15 citation statements)

References 77 publications

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“…The alveolar epithelium consists primarily of two types of alveolar epithelial cells: type I cells (ATI) and type II cells (ATII). ATI cells are involved primarily in gas exchange and maintenance of fluid balance [ 3 ]. The ATII cells are a major source of lung surfactant, they act as a progenitor cell population crucial for alveolar epithelium renewal, and they contribute to regulation of the immune/inflammatory responses within alveoli [ 4 , 5 , 6 , 7 , 8 ].…”

Section: Introductionmentioning

confidence: 99%

Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-κB Signaling

Vázquez‐Gómez

Karasová

Tylichová

et al. 2022

Cells

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Apart from its role in the metabolism of carcinogens, the aryl hydrocarbon receptor (AhR) has been suggested to be involved in the control of inflammatory responses within the respiratory tract. However, the mechanisms responsible for this are only partially known. In this study, we used A549 cell line, as a human model of lung alveolar type II (ATII)-like cells, to study the functional role of the AhR in control of inflammatory responses. Using IL-1β as an inflammation inducer, we found that the induction of cyclooxygenase-2 and secretion of prostaglandins, as well as expression and release of pro-inflammatory cytokines, were significantly higher in the AhR-deficient A549 cells. This was linked with an increased nuclear factor-κB (NF-κB) activity, and significantly enhanced phosphorylation of its regulators, IKKα/β, and their target IκBα, in the AhR-deficient A549 cells. In line with this, when we mimicked the exposure to a complex mixture of airborne pollutants, using an organic extract of reference diesel exhaust particle mixture, an exacerbated inflammatory response was observed in the AhR-deficient cells, as compared with wild-type A549 cells. Together, the present results indicate that the AhR may act as a negative regulator of the inflammatory response in the A549 model, via a direct modulation of NF-κB signaling. Its role(s) in the control of inflammation within the lung alveoli exposed to airborne pollutants, especially those which simultaneously activate the AhR, thus deserve further attention.

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Section: Introductionmentioning

confidence: 99%

Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-κB Signaling

Vázquez‐Gómez

Karasová

Tylichová

et al. 2022

Cells

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“…First, A549 cell lines were used in this study to establish the in vitro model of ALI. Studies have shown A549 is a suitable model for ATII cells because the long-term culture of A549 cells promotes a more ATII-like phenotype [ 38 ]. However, A549 is a human lung adenocarcinoma cell line that expresses different levels of oxidative stress compared to normal human ATII cells.…”

Section: Discussionmentioning

confidence: 99%

Nuclear factor-kappaB regulates the transcription of NADPH oxidase 1 in human alveolar epithelial cells

Zhu

et al. 2021

BMC Pulm Med

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Objective Acute lung injury (ALI) is characterized by inflammation and oxidative stress. Nuclear factor-kappaB (NF-κB) mediates the expression of various inflammation-related genes, including the NADPH oxidase family. This study aimed to identify the potential regulatory role of NF-κB on NADPH oxidases in tumor necrosis factor-α (TNF-α)-induced oxidative stress in human alveolar epithelial cells. Methods A549 cells were treated with TNF-α for 24 h to establish ALI cell models. RT-PCR, western blot, assessment of oxidative stress, Alibaba 2.1 online analysis, electrophoretic mobility shift assays and luciferase reporter analysis were employed to identify the potential regulatory role of NF-κB on NADPH oxidases in TNF-α-induced oxidative stress in human alveolar epithelial cells. Results The expression of NF-κB/p65 was notably upregulated in TNF-α-stimulated A549 cells. NF-κB knockdown by siRNA significantly inhibited the TNF-α-induced oxidative stress. Moreover, NF-κB/p65 siRNA could inhibit the activation of NOX1, NOX2 and NOX4 mRNA and protein expression in TNF-α-stimulated A549 cells. The next study demonstrated that NF-κB activated the transcription of NOX1 by binding to the -261 to -252 bp (NOX1/κB2, TAAAAATCCC) region of NOX1 promoter in TNF-α-stimulated A549 cells. Conclusion Our data demonstrated that NF-κB can aggravate TNF-α-induced ALI by regulating the oxidative stress response and the expression of NOX1, NOX2 and NOX4. Moreover, NF-κB could promote the NOX1 transcriptional activity via binding its promoter in TNF-α-stimulated A549 cells.

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“…But A549 is derived from a human lung adenocarcinoma cell line. [42] Also, the role that FERMT3 modulates cigarette smoke-induced EMT plays in airway remodeling, brosis, and malignant transformation may require further exploration. In addition, how FERMT3 regulates Wnt/β-Catenin signaling and whether FERMT3 affects other involving mechanisms needs further investigation.…”

Section: Discussionmentioning

confidence: 99%

FERMT3 Mediates Cigarette Smoke-induced Epithelial-mesenchymal Transition Through Wnt/β-Catenin Signaling

Chen

Lin

et al. 2021

Preprint

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Background: Cigarette smoking is a major risk factor for chronic obstructive pulmonary disease (COPD) and lung cancer. Epithelial-mesenchymal transition (EMT) is an essential pathophysiological process in COPD and plays an important role in airway remodeling, fibrosis, and malignant transformation of COPD. Previous studies have indicated FERMT3 is downregulated and plays a tumor suppressive role in lung cancer. However, the role of FERMT3 in COPD, including EMT, has not yet been investigated. Methods: The present study aimed to explore the potential role of FERMT3 in COPD and its underlying molecular mechanisms. Two GEO datasets were combined to identify FERMT3 involved in COPD. The expression of FERMT3 was identified in COPD from two GEO datasets. We then established EMT animal models and cell models through cigarette smoke (CS) or cigarette smoke extract (CSE) exposure to detect the expression of FERMT3 and EMT markers. RT-PCR, western blot, immunohistochemical, cell migration, and cell cycle were employed to investigate the potential regulatory effect of FERMT3 in CSE-induced EMT. Results: Based on the GEO dataset analysis, the expression of FERMT3 was downregulated in COPD-smoker bronchoalveolar lavage fluid than that in Non-smoker. Cigarette smoke exposure reduced the FERMT3 expression and induces EMT both in vivo and in vitro. The results showed that overexpression of FERMT3 could inhibit EMT induced by CSE in A549 cells. Furthermore, the CSE-induced cell migration and cell cycle progression were reversed by FERMT3 overexpression. Mechanistically, our study showed that overexpression of FERMT3 inhibited CSE-induced EMT through the Wnt/β-catenin signaling. Conclusions: In summary, these data suggest FERMT3 regulates cigarette smoke-induced epithelial-mesenchymal transition through Wnt/β-Catenin signaling. These findings indicated that FERMT3 was correlated with the development of COPD and may serve as a potential target for both COPD and lung cancer.

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Short-Term versus Long-Term Culture of A549 Cells for Evaluating the Effects of Lipopolysaccharide on Oxidative Stress, Surfactant Proteins and Cathelicidin LL-37

Cited by 19 publications

References 77 publications

Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-κB Signaling

Aryl Hydrocarbon Receptor (AhR) Limits the Inflammatory Responses in Human Lung Adenocarcinoma A549 Cells via Interference with NF-κB Signaling

Nuclear factor-kappaB regulates the transcription of NADPH oxidase 1 in human alveolar epithelial cells

FERMT3 Mediates Cigarette Smoke-induced Epithelial-mesenchymal Transition Through Wnt/β-Catenin Signaling

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