Diesel exhaust particles induce matrix metalloprotease-1 in human lung epithelial cells via a NADP(H) oxidase/NOX4 redox-dependent mechanism

Amara, Nadia; Bachoual, Rafik; Desmard, Mathieu; Gołda, Sławomir; Guichard, Cécile; Lanone, Sophie; Aubier, Michel; Ogier–Denis, Éric; Boczkowski, Jorge

doi:10.1152/ajplung.00445.2006

Cited by 86 publications

(80 citation statements)

References 45 publications

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“…The reasons for the preferential activation of MMP-2 in our work may be related to the influence of ROS on the activation of this enzyme, as previously demonstrated by us (42). However, we cannot exclude an effect of PM 2.5 on MMP-1 activity, as has been demonstrated in pulmonary alveolar epithelial cells (1).…”

Section: Discussionsupporting

confidence: 50%

Air pollution and cardiac remodeling: a role for RhoA/Rho-kinase

Zhao¹,

Yue²,

Xu³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

107

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Exposure to ambient air pollution has been associated with increases in blood pressure. We have previously demonstrated activation of the Rho/Rho kinase pathway in experimental hypertension in rats. In this investigation, we evaluated the effects of particulate matter of Ͻ2.5 m (PM2.5) exposure on cardiovascular responses and remodeling and tested the effect of Rho kinase inhibition on these effects. C57BL/6 mice were exposed to concentrated ambient PM2.5 or filtered air for 12 wk followed by a 14-day ANG II infusion in conjunction with fasudil, a Rho kinase antagonist, or placebo treatment. Blood pressure was monitored, followed by analysis of vascular function and ventricular remodeling indexes. PM 2.5 exposure potentiated ANG II-induced hypertension, and this effect was abolished by fasudil treatment. Cardiac and vascular RhoA activation was enhanced by PM 2.5 exposure along with increased expression of the guanine exchange factors (GEFs) PDZRhoGEF and p115 RhoGEF in PM 2.5-exposed mice. Parallel with increased RhoA activation, PM 2.5 exposure increased ANG II-induced cardiac hypertrophy and collagen deposition, with these increases being normalized by fasudil treatment. In conclusion, PM2.5 potentiates cardiac remodeling in response to ANG II through RhoA/ Rho kinase-dependent mechanisms. These findings have implications for the chronic cardiovascular health effects of air pollution. hypertension; vasoconstrictors; angiotensin II AMBIENT AIR POLLUTION mediated by fine particulate matter (PM) of Ͻ2.5 m in aerodynamic diameter (PM 2.5 ) has been associated with adverse cardiovascular outcomes (8,31,39,49). One important mechanism is the elevation in blood pressure (BP) that may occur within hours to days after exposure to high concentrations of PM 2.5 (6,16,21,52). Recent studies (21, 58) have shown that commonly encountered levels of airborne pollutants can result in a prohypertensive response in humans that may be exaggerated in predisposed individuals. This potentiating effect of inhaled particulates has been noted with other chronic conditions or risk factors such as atherosclerosis, diabetes, and postmenopausal status (31,40,49). Although the precise mechanisms remain elusive, there is increasing evidence that PM 2.5 exposure results in rapid changes in the vasculature (7, 32). We (51) have previously shown that PM 2.5 exposure results in the activation of RhoA/Rho-kinase (ROCK) through ROS pathways and hypothesized that this important signaling cascade may mediate at least some of the prohypertensive effects of PM 2.5 . Given the important role of RhoA/ ROCK in a multitude of processes, including the regulation of smooth muscle tone, cellular migration, and hypertrophy (36,47), in the present study we examined the effect of PM 2.5 exposure on vascular function and cardiac remodeling and tested the effects of ROCK antagonism.

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Section: Discussionsupporting

confidence: 50%

Air pollution and cardiac remodeling: a role for RhoA/Rho-kinase

Zhao¹,

Yue²,

Xu³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

107

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“…Quinones are important toxic compounds present in air pollution and abundant in all burnt organic material, including urban air particles, cigarette smoke, and diesel exhaust particles (DEP) [44]. DEP were reported to increase Nox4 ROS production after 1 h of incubation, suggesting the implication of Nox4 in the quinone metabolism [9]. Considering the structure/function relationship of the quinones used in this study (Table 2), we observed a dual stimulation/ inhibition effect that depends on their substitution state: Nox4 activity was stimulated by AA-861, duroquinone, tBuBQ, and tBuBHQ whereas other less substituted derivatives such as BQ, HQ, tMetBQ, and plumbagin, developed antioxidant properties ( Table 2).…”

Section: Discussionmentioning

confidence: 99%

“…Semiquinone radicals of inhaled airborne particulate matter are believed to cause oxidative stress by generating reactive oxygen species (ROS), as reported in the lung [8]. Furthermore, diesel exhaust particles composed of polycyclic aromatic hydrocarbons and quinones are involved in a cellular ROS production associated with lung function impairment via a Nox4 redox-dependent mechanism [9].…”

Section: Introductionmentioning

confidence: 99%

“…Nox4 is unique among other Nox isoenzymes in that its activity is constitutive and may depend on a specific conformation of the dehydrogenase DH domain that should allow a spontaneous transfer of electrons from NADPH to FAD and to the hemes [24,25]. Data from various studies indicated clearly that Nox4 activity is regulated at the mRNA level, implying that an increase or decrease of ROS production by Nox4 is correlated to an up regulation [9,16,[26][27][28][29][30][31][32][33] or to a decline [34] of Nox4 transcripts. Although it has not been reported yet, post-translational regulation of Nox4 oxidase activity cannot be excluded.…”

Section: Introductionmentioning

confidence: 99%

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Quinone compounds regulate the level of ROS production by the NADPH oxidase Nox4

Nguyen

Lardy

Rousset

et al. 2013

Biochemical Pharmacology

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NADPH oxidase Nox4 is expressed in a wide range of tissues and plays a role in cellular signaling by providing reactive oxygen species (ROS) as intracellular messengers. Nox4 oxidase activity is thought to be constitutive and regulated at the transcriptional level; however, we challenge this point of view and suggest that specific quinone derivatives could modulate this activity. In fact, we demonstrated a significant stimulation of Nox4 activity by 4 quinone derivatives (AA-861, tBuBHQ, tBuBQ, and duroquinone) observed in 3 different cellular models, HEK293E, T-REx™, and chondrocyte cell lines. Our results indicate that the effect is specific toward Nox4 versus Nox2. Furthermore, we showed that NAD(P)H:quinone oxidoreductase (NQO1) may participate in this stimulation. Interestingly, Nox4 activity is also stimulated by reducing agents that possibly act by reducing the disulfide bridge (Cys226, Cys270) located in the extracellular E-loop of Nox4. Such model of Nox4 activity regulation could provide new insight into the understanding of the molecular mechanism of the electron transfer through the enzyme, i.e., its potential redox regulation, and could also define new therapeutic targets in diseases in which quinones and Nox4 are implicated

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“…79 Amara et al could demonstrate that Diesel exhaust particles activate ERK1/2 which, combined with activation of the NADPH oxidase analog NOX4, modulate the expression and activity of the matrix metalloprotease (MMP)-1. 80 As a recent example, cerium oxide NPs were shown to elevate ROS levels leading to a strong induction of HO-1 via the p38-Nrf-2 ! signaling pathway in human bronchial epithelial cells (Beas-2B).…”

Section: The Role Of Oxidative Stress and Ros In Np Induced Signalingmentioning

confidence: 99%

Big Signals from Small Particles: Regulation of Cell Signaling Pathways by Nanoparticles

Rauch¹,

Kölch²,

et al. 2013

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Introduction 3391 2. Medical Applications of Nanomaterials 3391 2.1. Use of Nanomaterials in Diagnostic Applications 3392 3. Interaction of Nanomaterials with Living Cells 3392 3.1. Role of Physicochemical NP Properties in the Interaction between NPs and Biological Systems 3393 3.2. NP Uptake into the Cells 3393 3.2.1. Role of Size and Shape in NP Uptake 3393 3.2.2. Role of Surface Charge and Protein Corona on NP Uptake 3395 3.3. Activation of Signal Processing Pathways by NPs 3397 3.3.1. Interaction of NPs with Cell Membrane Receptors 3397 3.3.2. Role of Oxidative Stress and ROS in NP-Induced Signaling 3398 3.3.3. NPs Induce Cell Death Pathways 3400 3.3.4. Activation of Mechanotransduction Receptors by Magnetic NPs 3400 4. Magnetic NPs and Cell Signaling 3400 4.1. Controlled Activation of Cell Surface Receptors by Magnetic NPs 3400 4.1.1. Activation of Signal Transduction Receptors by Magnetic NPs 3400 4.1.2. Activation of Mechanotransduction Receptors and Mechanosensitive Signaling Pathways by Magnetic NPs 3400 4.2. Pathway Activation by Magnetic-NP-Induced Hyperthermia 3401 4.2.1. Molecular Targets of Hyperthermia: Heat Shock Proteins and p53 3401 5. Conclusions 3402 Author Information 3402 Corresponding Author 3402 Present Address 3402 Notes 3402 Biographies 3402 Acknowledgments 3403 References 3403

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Diesel exhaust particles induce matrix metalloprotease-1 in human lung epithelial cells via a NADP(H) oxidase/NOX4 redox-dependent mechanism

Cited by 86 publications

References 45 publications

Air pollution and cardiac remodeling: a role for RhoA/Rho-kinase

Air pollution and cardiac remodeling: a role for RhoA/Rho-kinase

Quinone compounds regulate the level of ROS production by the NADPH oxidase Nox4

Big Signals from Small Particles: Regulation of Cell Signaling Pathways by Nanoparticles

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