Smad3 mediates cigarette smoke extract (CSE) induction of VEGF release by human fetal lung fibroblasts

Farid, Maha; Kanaji, Nobuhiro; Nakanishi, Masayoshi; Gunji, Yoko; Michalski, Joel; Iwasawa, Shunichiro; Ikari, Jun; Wang, Xingqi; Basma, Hesham; Nelson, Amy; Liu, Xiangde; Rennard, Stephen I.

doi:10.1016/j.toxlet.2013.04.011

Cited by 22 publications

(17 citation statements)

References 18 publications

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“…Contrary to our expectations, CSE increased VEGF release from bronchial epithelial cells in this study. CSE-induced VEGF release was also observed in human lung fibroblast, suggesting that it is not cell type-specific (27). Then, considering the increased VEGF release from epithelial cells by CSE, how does VEGF downregulation occur in the lung parenchyma of COPD patients?…”

Section: Discussionmentioning

confidence: 99%

Neutrophil Elastase Differentially Regulates Interleukin 8 (IL-8) and Vascular Endothelial Growth Factor (VEGF) Production by Cigarette Smoke Extract

Lee

Jeong

et al. 2015

Journal of Biological Chemistry

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Background: Interaction between oxidative stress (CSE) and protease (NE) may contribute to COPD pathogenesis. Results: Although NE enhances CSE-induced IL-8, it suppresses VEGF production, which is due to degradation by uptake of NE into bronchial epithelial cells. Conclusion: NE contributes to the pathogenesis of COPD by enhancing inflammation and apoptosis.Significance: This provides a molecular mechanism for understanding COPD pathogenesis.

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Section: Discussionmentioning

confidence: 99%

Neutrophil Elastase Differentially Regulates Interleukin 8 (IL-8) and Vascular Endothelial Growth Factor (VEGF) Production by Cigarette Smoke Extract

Lee

Jeong

et al. 2015

Journal of Biological Chemistry

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“…Cigarette smoke extract (CSE) treatment significantly induces interleukin-8 (IL-8) and transforming growth factor-beta 1 (TGF-β1) production and profoundly suppresses the proliferation and growth of erythroid and granulocyte-macrophage progenitors (6). Stimulation with CSE in human lung fibroblast cells induces the expression of phosphorylated Smad3, a main downstream target of the TGF-β1 receptor, which results in the secretion of vascular endothelial growth factor (VEGF) (7). CSE increases the migratory and invasive activity of ovarian cancer cells and induces the expression of the EMT-related transcriptional factors Snail and Slug (8).…”

mentioning

confidence: 99%

PI3K Catalytic Isoform Alteration Promotes the LIMK1-related Metastasis Through the PAK1 or ROCK1/2 Activation in Cigarette Smoke-exposed Ovarian Cancer Cells

2017

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“…CSE was prepared from Daqingshan cigarettes (Tar: 12.5, Hohhot Cigarette Factory, Hohhot, China; model group) as previously described [15]. A 1 cm cigarette without lter was combusted with a variable speed pump (Thermo Fisher Scienti c, Waltham, MA, USA).…”

Section: Preparation Of Csementioning

confidence: 99%

Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways

Zhang¹,

Wang²,

Liu³

et al. 2020

Preprint

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Chronic obstructive pulmonary disease (COPD) is a common respiratory disease associated with inflammation and oxidative stress. Sappanone A (SA) is a homoisoflavanone that has been proven to have anti-inflammatory and anti-oxidant effects. However, the role of SA in COPD remains unclear. Thus, the present study was aimed to evaluate the beneficial effect of SA on COPD in vitro. The human bronchial epithelial cells were exposed to 5% cigarette smoke extracts (CSE) to induce an in vitro model of COPD. Our results showed that SA treatment significantly attenuated the CSE-caused induction of ROS and reduction of SOD and GPx activities in 16HBE cells. In addition, SA inhibited the production of inflammatory cytokines IL-6, IFN-γ, and TNF-α in CSE-stimulated 16HBE cells. Moreover, the CSE-stimulated cell apoptosis of 16HBE cells were abrogated by SA. Furthermore, we observed that SA treatment greatly promoted the activation of Nrf2/HO-1 signaling pathway, as well as inhibited the activation of TLR4/NF-κB signaling pathway in CSE-stimulated 16HBE cells. Subsequent rescue assay revealed that the protective effects of SA on CSE-stimulated 16HBE cells were reversed by Nrf2 knockdown or TLR4 overexpression. Taken together, these findings demonstrated that SA inhibits oxidative stress, inflammation and apoptosis in CSE-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways.

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Smad3 mediates cigarette smoke extract (CSE) induction of VEGF release by human fetal lung fibroblasts

Cited by 22 publications

References 18 publications

Neutrophil Elastase Differentially Regulates Interleukin 8 (IL-8) and Vascular Endothelial Growth Factor (VEGF) Production by Cigarette Smoke Extract

Neutrophil Elastase Differentially Regulates Interleukin 8 (IL-8) and Vascular Endothelial Growth Factor (VEGF) Production by Cigarette Smoke Extract

PI3K Catalytic Isoform Alteration Promotes the LIMK1-related Metastasis Through the PAK1 or ROCK1/2 Activation in Cigarette Smoke-exposed Ovarian Cancer Cells

Sappanone A inhibits oxidative stress, inflammation and apoptosis in cigarette smoke-induced human bronchial epithelial cells through regulating Nrf2/HO-1 and TLR4/NF-κB signaling pathways

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