Environmental Tobacco Smoke Suppresses Nuclear Factor-κB Signaling to Increase Apoptosis in Infant Monkey Lungs

Zhong, Caiyun; Zhou, Yuhao; Joad, Jesse P.; Pinkerton, Kent E.

doi:10.1164/rccm.200503-509oc

Cited by 27 publications

(24 citation statements)

References 70 publications

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“…Exposure to SHS during the perinatal period suppresses NF-k B activity in the neonatal nonhuman primate and exposure to mainstream cigarette smoke inhibits NF-k B in human monocytes. 32,33 Conversely, exposure to cigarette smoke increases NF-k B activity in vitro. 34 Th ese observations suggest that cigarette smoke-mediated activation of NF-k B is tissue specifi c. Interestingly, despite an overall increase in endothelial NF-k B expression in passive smokers, we observed that prolonged exposure to SHS ( .…”

Section: Figure 1 -Expression Of Markers Of Endothelial Reactivity Imentioning

confidence: 99%

Secondhand Smoking Is Associated With Vascular Inflammation

Adams

Wan

Wei

et al. 2015

Chest

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Section: Figure 1 -Expression Of Markers Of Endothelial Reactivity Imentioning

confidence: 99%

Secondhand Smoking Is Associated With Vascular Inflammation

Adams

Wan

Wei

et al. 2015

Chest

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“…Both epithelial cells and endothelial cells die, and their apoptosis has been demonstrated in human and animal lungs (34,62,(91)(92)(93). The loss of alveolar capillary endothelial cells and of small capillaries (94) de facto makes emphysema also a vascular disease (95)(96)(97)(98)(99).…”

Section: No Vegf No Growth -Only Deathmentioning

confidence: 99%

Molecular pathogenesis of emphysema

Taraseviciene‐Stewart

Voelkel²

2008

J. Clin. Invest.

227

184

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Emphysema is one manifestation of a group of chronic, obstructive, and frequently progressive destructive lung diseases. Cigarette smoking and air pollution are the main causes of emphysema in humans, and cigarette smoking causes emphysema in rodents. This review examines the concept of a homeostatically active lung structure maintenance program that, when attacked by proteases and oxidants, leads to the loss of alveolar septal cells and airspace enlargement. Inflammatory and noninflammatory mechanisms of disease pathogenesis, as well as the role of the innate and adaptive immune systems, are being explored in genetically altered animals and in exposure models of this disease. These recent scientific advances support a model whereby alveolar destruction resulting from a coalescence of mechanical forces, such as hyperinflation, and more recently recognized cellular and molecular events, including apoptosis, cellular senescence, and failed lung tissue repair, produces the clinically recognized syndrome of emphysema.

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“…NF-κB is the major transcription factor that controls the apoptotic process and regulates the transcription of a broad range of gene products (Zhong et al 2006), including those activated in response to various oxidative stresses, being crucially involved in inflammation, apoptosis, and proliferation in lung tissue (Dagher et al 2006;Valença et al 2006). NF-κB has also been shown to be stimulated in response to diverse pathogenic particles (Churg et al 2005;Dagher et al 2007;Park and Christman 2006;Pourazar et al 2005;Takizawa et al 1999;Takizawa 2004;Valença et al 2006;Zhong et al 2006).…”

Section: Activation Of the Mapk Cascades And Transcription Factorsmentioning

confidence: 99%

Roles of oxidative stress in signaling and inflammation induced by particulate matter

et al. 2010

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This review reports the role of oxidative stress in impairing the function of lung exposed to particulate matter (PM). PM constitutes a heterogeneous mixture of various types of particles, many of which are likely to be involved in oxidative stress induction and respiratory diseases. Probably, the ability of PM to cause oxidative stress underlies the association between increased exposure to PM and exacerbations of lung disease. Mostly because of their large surface area, ultrafine particles have been shown to cause oxidative stress and proinflammatory effects in different in vivo and in vitro studies. Particle components and surface area may act synergistically inducing lung inflammation. In this vein, reactive oxygen species elicited upon PM exposure have been shown to activate a number of redox-responsive signaling pathways and Ca(2+) influx in lung target cells that are involved in the expression of genes that modulate relevant responses to lung inflammation and disease.

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Environmental Tobacco Smoke Suppresses Nuclear Factor-κB Signaling to Increase Apoptosis in Infant Monkey Lungs

Cited by 27 publications

References 70 publications

Secondhand Smoking Is Associated With Vascular Inflammation

Secondhand Smoking Is Associated With Vascular Inflammation

Molecular pathogenesis of emphysema

Roles of oxidative stress in signaling and inflammation induced by particulate matter

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