ArticleBMC pulmonary medicine2021
Nuclear factor-kappaB regulates the transcription of NADPH oxidase 1 in human alveolar epithelial cells.
Article in BMC pulmonary medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
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- Physical Activity and Cancer Incidence and Mortality: Current Evidence and Biological Mechanisms.Cancers · 2025Review
- Comparative Effects of Tumor Necrosis Factor Alpha, Lipopolysaccharide, and Palmitate on Mitochondrial Dysfunction in Cultured 3T3-L1 Adipocytes.Cell biochemistry and biophysics · 2025Article
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- Extracellular Vesicles fromMarine drugs · 2024Article
- Role of the CCL5 and Its Receptor, CCR5, in the Genesis of Aldosterone-Induced Hypertension, Vascular Dysfunction, and End-Organ Damage.Hypertension (Dallas, Tex. : 1979) · 2024Article
- Cigarette Smoke-Induced Reactive Oxygen Species Formation: A Concise Review.Antioxidants (Basel, Switzerland) · 2023Review
- Role of NADPH Oxidase 4 in Corneal Endothelial Cells Is Mediated by Endoplasmic Reticulum Stress and Autophagy.Antioxidants (Basel, Switzerland) · 2023Article
- NADPH oxidase and endoplasmic reticulum stress is associated with neuronal degeneration in orbitofrontal cortex of individuals with alcohol use disorder.Addiction biology · 2023Article
- The role of glutathione peroxidase-1 in health and disease.Free radical biology & medicine · 2022Review
- The protective effect of natural medicines against excessive inflammation and oxidative stress in acute lung injury by regulating the Nrf2 signaling pathway.Frontiers in pharmacology · 2022Review
- The Role of Nuclear Factor-κB in Cancer Immunity and Immunoediting.Cancer control : journal of the Moffitt Cancer CenterReview
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
objectiveAcute 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.
methodsA549 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.
resultsThe 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.
conclusionOur 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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