Bim mediates mitochondria‐regulated particulate matter‐induced apoptosis in alveolar epithelial cells

Zhang, J.; Ghio, Andrew J.; Chang, Wenteh; Kamdar, Opal; Rosen, Glenn D.; Upadhyay, Daya

doi:10.1016/j.febslet.2007.07.080

Cited by 15 publications

(24 citation statements)

References 23 publications

(46 reference statements)

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“…Our results were obtained with a low concentration of PM 2.5 unlike previous publications performed with higher doses (e.g. 100 μg/cm 2 , [18]). Indeed, the standard dose used here (10 μg/cm 2 ) is a concentration which could mimic a five day exposure of PM 2.5 in the tracheobronchial region, considering that PM 2.5 mass deposition is 2.3 μg/cm 2 /24 h [11].…”

Section: Discussioncontrasting

confidence: 56%

“…The activation of caspases or other proteases triggers the proteolysis of specific substrates involved into the final appearance of morphological features of apoptosis. Most publications dealing with toxicity of airborne particles showed an induction of apoptosis associated with ROS generation, ΔΨm drop, caspase-9 activation and DNA fragmentation [18].…”

Section: Introductionmentioning

confidence: 99%

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Polycyclic aromatic hydrocarbon components contribute to the mitochondria-antiapoptotic effect of fine particulate matter on human bronchial epithelial cells via the aryl hydrocarbon receptor

et al. 2011

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Section: Discussioncontrasting

confidence: 56%

Section: Introductionmentioning

confidence: 99%

Polycyclic aromatic hydrocarbon components contribute to the mitochondria-antiapoptotic effect of fine particulate matter on human bronchial epithelial cells via the aryl hydrocarbon receptor

et al. 2011

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“…Furthermore, IB3‐1 CF cells were found to be highly sensitive to PM‐induced oxidative stress and apoptosis at much lower dose (25 μg/cm 2 ), as compared to previously reported PM‐induced apoptosis in alveolar epithelial cells (AEC) and A549 cells at the dose of 100 μg/cm 2 [6,17]. Therefore, a dose of 25 μg/cm 2 was used to perform all further experiments in IB3‐1 cells.…”

Section: Resultsmentioning

confidence: 76%

Air pollution induces enhanced mitochondrial oxidative stress in cystic fibrosis airway epithelium

Kamdar¹,

Le²,

Zhang³

et al. 2008

FEBS Letters

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We studied the effects of airborne particulate matters (PM) on cystic fibrosis (CF) epithelium. We noted that PM enhanced human CF bronchial epithelial apoptosis, activated caspase-9 and PARP-1; and reduced mitochondrial membrane potential. Mitochondrial inhibitors (4,4-diisothiocyanatostilbene-2,2 0 disulfonic acid, rotenone and thenoyltrifluoroacetone) blocked PM-induced generation of reactive oxygen species and apoptosis. PM upregulated pro-apoptotic Bad, Bax, p53 and p21; and enhanced mitochondrial localization of Bax. The antiapoptotic Bcl-2, Bcl-xl, Mcl-1 and Xiap remained unchanged; however, overexpression of Bcl-xl blocked PM-induced apoptosis. Accordingly, we provide the evidence that PM enhances oxidative stress and mitochondrial signaling mediated apoptosis via the modulation of Bcl family proteins in CF.

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“…Numerous PM exposures activate the same kinases and pro-inflammatory transcription factors observed with cigarette smoke 115–118. Comparable to cigarette smoke, the same particles subsequently affect a release of inflammatory and apoptotic mediators 119–124…”

Section: Mechanism Of Injury Following Particle Exposuresmentioning

confidence: 94%

Lung injury after cigarette smoking is particle related

Sangani¹,

Ghio

2011

COPD

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The specific component responsible and the mechanistic pathway for increased human morbidity and mortality after cigarette smoking are yet to be delineated. We propose that 1) injury and disease following cigarette smoking are associated with exposure to and retention of particles produced during smoking and 2) the biological effects of particles associated with cigarette smoking share a single mechanism of injury with all particles. Smoking one cigarette exposes the human respiratory tract to between 15,000 and 40,000 μg particulate matter; this is a carbonaceous product of an incomplete combustion. There are numerous human exposures to other particles, and these vary widely in composition, absolute magnitude, and size of the particle. Individuals exposed to all these particles share a common clinical presentation with a loss of pulmonary function, increased bronchial hyperresponsiveness, pathologic changes of emphysema and fibrosis, and comorbidities, including cardiovascular disease, cerebrovascular disease, peripheral vascular disease, and cancers. Mechanistically, all particle exposures produce an oxidative stress, which is associated with a series of reactions, including an activation of kinase cascades and transcription factors, release of inflammatory mediators, and apoptosis. If disease associated with cigarette smoking is recognized to be particle related, then certain aspects of the clinical presentation can be predicted; this would include worsening of pulmonary function and progression of pathological changes and comorbidity (eg, emphysema and carcinogenesis) after smoking cessation since the particle is retained in the lung and the exposure continues.

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Bim mediates mitochondria‐regulated particulate matter‐induced apoptosis in alveolar epithelial cells

Cited by 15 publications

References 23 publications

Polycyclic aromatic hydrocarbon components contribute to the mitochondria-antiapoptotic effect of fine particulate matter on human bronchial epithelial cells via the aryl hydrocarbon receptor

Polycyclic aromatic hydrocarbon components contribute to the mitochondria-antiapoptotic effect of fine particulate matter on human bronchial epithelial cells via the aryl hydrocarbon receptor

Air pollution induces enhanced mitochondrial oxidative stress in cystic fibrosis airway epithelium

Lung injury after cigarette smoking is particle related

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