The MAPKinase Signaling and the Stimulatory Protein-1 (Sp1) Transcription Factor Are Involved in the Phototherapy Effect on Cytokines Secretion from Human Bronchial Epithelial Cells Stimulated with Cigarette Smoke Extract

Brito, Auriléia Aparecida de; Herculano, Karine Zanella; Miranda, Michelle B.; Sá, Ana Karolina; Carvalho, José A.M.; Albertini, Regiane; Hc, Castro-Faria-Neto; Oliveira, Ana Paula Ligeiro de; Aimbire, Flávio

doi:10.1007/s10753-021-01448-5

Cited by 4 publications

(13 citation statements)

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“…Prolonged exposure to CS promotes aberrant inflammatory responses in the airways, leading to tissue remodeling and subsequent reduction of airflow, which are the main features of COPD [16,27]. Oxidative stress generated by exposure to CS is responsible for exacerbated inflammation in the bronchial human epithelium [17,30].…”

Section: Molecular Alterations Induced By Cs Exposurementioning

confidence: 99%

“…Oxidative stress generated by exposure to CS is responsible for exacerbated inflammation in the bronchial human epithelium [17,30]. Bronchial epithelial cells are the main source of cytokines, chemokines and adhesion molecules in the CS-exposed lung, modulating airway wall functionality and immune responses [27]. They respond to CSE by activating multiple inflammatory pathways, including mitogen-activated protein kinases (MAPKs), leading to the activation of extracellular signal-regulated kinases (ERK1/2), p38 and c-Jun N-terminal kinase (JNK) and the transcriptional factor nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) (Figure 3).…”

Section: Molecular Alterations Induced By Cs Exposurementioning

confidence: 99%

“…TLR4 expression is increased in response to CSE [84], and its activation triggers most of the CSE-induced proinflammatory pathways in HBE cells. In HBEs, NF-κB, the master regulator of transcriptional reprogramming during inflammation, was widely demonstrated to regulate the inflammatory response to CSE [17,22,24,27,32,36,42,45,70,77,78,98,99,112].…”

Section: Inflammatory Pathwaysmentioning

confidence: 99%

“…Additionally, stimulation of HBEs with CSE leads to activation of MAPKs, which is associated with proliferation, cell survival and motility, and cellular metabolism, and drives stress response and inflammation. More specifically, among MAPKs, activation of c-Jun N-terminal kinase (JNK), p38 and ERK1/2 has been widely described in relation to CSE-induced inflammation [22,27,29,36,46,49,53,74,77,83,86,88,98,[102][103][104]113].…”

Section: Inflammatory Pathwaysmentioning

confidence: 99%

“…As is well known, the activation of these pathways leads to increased levels of pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6, and IL-8. Of note, these cytokines are key mediators of CS-induced lung inflammation as well [17,19,22,24,25,[27][28][29][30]32,33,36,37,40,42,[44][45][46][69][70][71]74,75,[77][78][79][80][81]83,90,98,99,102,104,112,113]. ROS, increased by CS, enhance the activation of the IκB kinase (IKK) complex (IKKβ, IKKα, and NF-κB essential modulator (NEMO), leading to the phosphorylation, ubiquitination and proteasomal degradation of IκB, in particular IκBα.…”

Section: Inflammatory Pathwaysmentioning

confidence: 99%

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Cellular and Molecular Signatures of Oxidative Stress in Bronchial Epithelial Cell Models Injured by Cigarette Smoke Extract

Cipollina

Bruno

Fasola

et al. 2022

IJMS

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Exposure of the airways epithelium to environmental insults, including cigarette smoke, results in increased oxidative stress due to unbalance between oxidants and antioxidants in favor of oxidants. Oxidative stress is a feature of inflammation and promotes the progression of chronic lung diseases, including Chronic Obstructive Pulmonary Disease (COPD). Increased oxidative stress leads to exhaustion of antioxidant defenses, alterations in autophagy/mitophagy and cell survival regulatory mechanisms, thus promoting cell senescence. All these events are amplified by the increase of inflammation driven by oxidative stress. Several models of bronchial epithelial cells are used to study the molecular mechanisms and the cellular functions altered by cigarette smoke extract (CSE) exposure, and to test the efficacy of molecules with antioxidant properties. This review offers a comprehensive synthesis of human in-vitro and ex-vivo studies published from 2011 to 2021 describing the molecular and cellular mechanisms evoked by CSE exposure in bronchial epithelial cells, the most used experimental models and the mechanisms of action of cellular antioxidants systems as well as natural and synthetic antioxidant compounds.

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Section: Molecular Alterations Induced By Cs Exposurementioning

confidence: 99%

Section: Molecular Alterations Induced By Cs Exposurementioning

confidence: 99%

Section: Inflammatory Pathwaysmentioning

confidence: 99%

Section: Inflammatory Pathwaysmentioning

confidence: 99%

Section: Inflammatory Pathwaysmentioning

confidence: 99%

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Cellular and Molecular Signatures of Oxidative Stress in Bronchial Epithelial Cell Models Injured by Cigarette Smoke Extract

Cipollina

Bruno

Fasola

et al. 2022

IJMS

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Photobiomodulation mitigates Bothrops jararacussu venom-induced damage in myoblast cells by enhancing myogenic factors and reducing cytokine production

Silva,

Gouveia,

Campos

et al. 2024

PLoS Negl Trop Dis

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Background Photobiomodulation has exhibited promise in mitigating the local effects induced by Bothrops snakebite envenoming; however, the mechanisms underlying this protection are not yet fully understood. Herein, the effectiveness of photobiomodulation effects on regenerative response of C2C12 myoblast cells following exposure to Bothrops jararacussu venom (BjsuV), as well as the mechanisms involved was investigated. Methodology/Principal findings C2C12 myoblast cells were exposed to BjsuV (12.5 μg/mL) and irradiated once for 10 seconds with laser light of 660 nm (14.08 mW; 0.04 cm2; 352 mW/cm2) or 780 nm (17.6 mW; 0.04 cm2; 440 mW/ cm2) to provide energy densities of 3.52 and 4.4 J/cm2, and total energies of 0.1408 and 0.176 J, respectively. Cell migration was assessed through a wound-healing assay. The expression of MAPK p38-α, NF-Кβ, Myf5, Pax-7, MyoD, and myogenin proteins were assessed by western blotting analysis. In addition, interleukin IL1-β, IL-6, TNF-alfa and IL-10 levels were measured in the supernatant by ELISA. The PBM applied to C2C12 cells exposed to BjsuV promoted cell migration, increase the expression of myogenic factors (Pax7, MyF5, MyoD and myogenin), reduced the levels of proinflammatory cytokines, IL1-β, IL-6, TNF-alfa, and increased the levels of anti-inflammatory cytokine IL-10. In addition, PBM downregulates the expression of NF-kB, and had no effect on p38 MAKP. Conclusion/Significance These data demonstrated that protection of the muscle cell by PBM seems to be related to the increase of myogenic factors as well as the modulation of inflammatory mediators. PBM therapy may offer a new therapeutic strategy to address the local effects of snakebite envenoming by promoting muscle regeneration and reducing the inflammatory process.

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Identification of Ferroptosis-Related Hub Genes and Their Association with Immune Infiltration in Chronic Obstructive Pulmonary Disease by Bioinformatics Analysis

Yang¹,

Zhang²,

Liu³

et al. 2022

COPD

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The MAPKinase Signaling and the Stimulatory Protein-1 (Sp1) Transcription Factor Are Involved in the Phototherapy Effect on Cytokines Secretion from Human Bronchial Epithelial Cells Stimulated with Cigarette Smoke Extract

Cited by 4 publications

References 50 publications

Cellular and Molecular Signatures of Oxidative Stress in Bronchial Epithelial Cell Models Injured by Cigarette Smoke Extract

Cellular and Molecular Signatures of Oxidative Stress in Bronchial Epithelial Cell Models Injured by Cigarette Smoke Extract

Photobiomodulation mitigates Bothrops jararacussu venom-induced damage in myoblast cells by enhancing myogenic factors and reducing cytokine production

Identification of Ferroptosis-Related Hub Genes and Their Association with Immune Infiltration in Chronic Obstructive Pulmonary Disease by Bioinformatics Analysis

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