Jorge Boczkowski

Université Paris-Est Créteil Val de Marne - Université Paris 12, Créteil, Île-de-France, France

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Publications (184)778.68 Total impact

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    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is often associated with age-related systemic abnormalities that adversely affect the prognosis. Whether these manifestations are linked to the lung alterations or are independent complications of smoking remains unclear. To look for aging-related systemic manifestations and telomere shortening in COPD patients and smokers with minor lung destruction responsible for a decline in the diffusing capacity for carbon monoxide (DLCO) corrected for alveolar volume (KCO). Cross-sectional study in 301 individuals (100 with COPD, 100 smokers without COPD, and 101 nonsmokers without COPD). Compared to control smokers, patients with COPD had higher aortic pulse-wave velocity (PWV), lower bone mineral density (BMD) and appendicular skeletal muscle mass index (ASMMI), and shorter telomere length (TL). Insulin resistance (HOMA-IR) and glomerular filtration rate (GFR) were similar between control smokers and COPD patients. Smokers did not differ from nonsmokers for any of these parameters. However, smokers with normal spirometry but low KCO had lower ASMMI values compared to those with normal KCO. Moreover, female smokers with low KCO, had lower BMD and shorter TL compared to those with normal KCO. Aging-related abnormalities in patients with COPD are also found in smokers with minor lung dysfunction manifesting as a KCO decrease. Decreased KCO might be useful, particularly among women, for identifying smokers at high risk for aging-related systemic manifestations and telomere shortening.
    PLoS ONE 01/2015; 10(3):e0121539. DOI:10.1371/journal.pone.0121539 · 3.53 Impact Factor
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    ABSTRACT: Alteration of functional regenerative properties of parenchymal lung fibroblasts is widely proposed as a pathogenic mechanism for chronic obstructive pulmonary disease (COPD). However, what these functions are and how they are impaired in COPD remain poorly understood. Apart from the role of fibroblasts in producing extracellular matrix, recent studies in organs different from the lung suggest that such cells might contribute to repair processes by acting like mesenchymal stem cells. In addition, several reports sustain that the Hedgehog pathway is altered in COPD patients thus aggravating the disease. Nevertheless, whether this pathway is dysregulated in COPD fibroblasts remains unknown. We investigated the stem cell features and the expression of Hedgehog components in human lung fibroblasts isolated from histologically-normal parenchymal tissue from 25 patients-8 non-smokers/non-COPD, 8 smokers-non COPD and 9 smokers with COPD-who were undergoing surgery for lung tumor resection. We found that lung fibroblasts resemble mesenchymal stem cells in terms of cell surface marker expression, differentiation ability and immunosuppressive potential and that these properties were altered in lung fibroblasts from smokers and even more in COPD patients. Furthermore, we showed that some of these phenotypic changes can be explained by an over activation of the Hedgehog signaling in smoker and COPD fibroblasts. Our study reveals that lung fibroblasts possess mesenchymal stem cell-features which are impaired in COPD via the contribution of an abnormal Hedgehog signaling. These processes should constitute a novel pathomechanism accounting for disease occurrence and progression.
    PLoS ONE 01/2015; 10(3):e0121579. DOI:10.1371/journal.pone.0121579 · 3.53 Impact Factor
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    ABSTRACT: -Cells exhibiting dysregulated growth may express telomerase reverse transcriptase (TERT), whose dual function consists in maintaining telomere length, in association with the RNA template molecule TERC and controlling cell growth. Here, we investigated lung TERT in human and experimental pulmonary hypertension (PH) and its role in controlling pulmonary artery-smooth muscle cell (PA-SMC) proliferation. -Marked TERT expression and/or activity were found in lungs from patients with idiopathic PH and from mice with PH induced by hypoxia or serotonin-transporter overexpression (SM22-5HTT+ mice), chiefly within PA-SMCs. In cultured mouse PA-SMCs, TERT was expressed upon growth stimulation by serum. The TERT inhibitor imetelstat and the TERT activator TA65 abrogated and stimulated PA-SMC growth, respectively. PA-SMCs from PH mice showed a heightened proliferative phenotype associated with increased TERT expression, which was suppressed by imetelstat treatment. TERC(-/-) mice at generation 2 (G2) and TERT(-/-) mice at G2, G3, and G4 developed less severe PH than did wild-type mice exposed to chronic hypoxia, with less distal pulmonary-artery muscularization and fewer Ki67-stained proliferating PA-SMCs. Telomere length differed between TERC(-/-) and TERT(-/-) mice, whereas PH severity was similar in the two strains and across generations. Chronic imetelstat treatment reduced hypoxia-induced PH in wild-type mice or partially reversed established PH in SM22-5HTT+ mice, while simultaneously decreasing TERT expression. Opposite effects occurred in mice treated with TA65. -Telomerase exerts telomere-independent effects on PA-SMC growth in PH and may constitute a treatment target for PH.
    Circulation 12/2014; DOI:10.1161/CIRCULATIONAHA.114.013258 · 14.95 Impact Factor
  • L Boyer, L Savale, J Boczkowski, S Adnot
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    ABSTRACT: The biological mechanisms of aging, and more specifically cellular senescence, are increasingly a subject of research. Cellular senescence may be a common determinant of many age-related diseases, including some chronic lung diseases such as chronic obstructive pulmonary disease (COPD) or idiopathic pulmonary fibrosis. Many arguments suggest that these diseases are associated with premature senescence of lung cells, which may be involved in the pathophysiology of respiratory alterations. Furthermore, these diseases are associated with systemic manifestations, such as bone loss, muscle wasting and atherosclerosis, which impact on symptoms and prognosis. Whether these alterations are related to a common pathogenic mechanism or develop independently in patients with COPD remains an open question. In this review, we will focus on cellular senescence and COPD. Two concepts will be discussed: (1) the role of cell senescence in the pathophysiology of lung destruction, vascular remodeling and inflammation in COPD, (2) the possible link between the pulmonary and systemic manifestations of COPD which could reflect a general process of accelerated aging. Copyright © 2014 SPLF. Published by Elsevier Masson SAS. All rights reserved.
  • L. Boyer, L. Savale, J. Boczkowski, S. Adnot
    Revue des Maladies Respiratoires 11/2014; DOI:10.1016/j.rmr.2014.07.015 · 0.49 Impact Factor
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    ABSTRACT: We hypothesized that O2 tension influences the redox state and the immunomodulatory responses of inflammatory cells to dimethyl fumarate (DMF), an activator of the nuclear factor Nrf2 that controls antioxidant genes expression. This concept was investigated in macrophages permanently cultured at either physiological (5% O2) or atmospheric (20% O2) oxygen levels and then treated with DMF or challenged with lipopolysaccharide (LPS) to induce inflammation. RAW 264.7 macrophages cultured at 20% O2 exhibited a pro-oxidant phenotype, reflected by a lower content of reduced glutathione, higher oxidized glutathione and increased production of reactive oxygen species when compared to macrophages continuously grown at 5% O2. At 20% O2, DMF induced a stronger antioxidant response compared to 5% O2 as evidenced by a higher expression of heme oxygenase-1, NAD(P)H:quinone oxydoreductase-1 and superoxide dismutase-2. After challenge of macrophages with LPS, several pro-inflammatory (iNOS, TNF-α, MMP-2, MMP-9), anti-inflammatory (arginase-1, IL-10) and pro-angiogenic (VEGF-A) mediators were evaluated in the presence or absence of DMF. All markers, with few interesting exceptions, were significantly reduced at 5% O2. This study brings new insights on the effects of O2 in the cellular adaptation to oxidative and inflammatory stimuli and highlights the importance of characterizing the effects of chemicals and drugs at physiologically relevant O2 tension. Our results demonstrate that the common practice of culturing cells at atmospheric O2 drives the endogenous cellular environment towards an oxidative stress phenotype, affecting inflammation and the expression of antioxidant pathways by exogenous modulators. J. Cell. Physiol. © 2014 Wiley Periodicals, Inc.
    Journal of Cellular Physiology 10/2014; DOI:10.1002/jcp.24844 · 3.87 Impact Factor
  • Revue des Maladies Respiratoires 09/2014; 31(7):655. DOI:10.1016/j.rmr.2014.04.025 · 0.49 Impact Factor
  • Revue des Maladies Respiratoires 09/2014; 31(7):660–661. DOI:10.1016/j.rmr.2014.04.037 · 0.49 Impact Factor
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    ABSTRACT: Manufactured nanomaterials (MNMs) have the potential to improve everyday life as they can be utilised in numerous medical applications and day-to-day consumer products. However, this increased use has led to concerns about the potential environmental and human health impacts. The protein p53 is a key transcription factor implicated in cellular defence and reparative responses to various stress factors. Additionally, p53 has been implicated in cellular responses following exposure to some MNMs. Here, the role of the MNM mediated p53 induction and activation and its downstream effects following exposure to five well-characterised materials [namely two types of TiO2, two carbon black (CB), and one single-walled carbon nanotube (SWCNT)] were investigated. MNM internalisation, cellular viability, p53 protein induction and activation, oxidative stress, inflammation and apoptosis were measured in murine cell line and primary pulmonary macrophage models. It was observed that p53 was implicated in the biological responses to MNMs, with oxidative stress associated with p53 activation (only following exposure to the SWCNT). We demonstrate that p53 acted as an antioxidant and anti-inflammatory in macrophage responses to SWCNT and CB NMs. However, p53 was neither involved in MNM-induced cellular toxicity, nor in the apoptosis induced by these MNMs. Moreover, the physicochemical characteristics of MNMs seemed to influence their biological effects-SWCNT the materials with the largest surface area and a fibrous shape were the most cytotoxic in this study and were capable of the induction and activation of p53.
    Archive für Toxikologie 08/2014; DOI:10.1007/s00204-014-1324-5 · 5.08 Impact Factor
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    ABSTRACT: BackgroundAlthough major concerns exist regarding the potential consequences of human exposure to nanoparticles (NP), no human toxicological data is currently available. To address this issue, we took welders, who present various adverse respiratory outcomes, as a model population of occupational exposure to NP.The aim of this study was to evaluate if welding fume-issued NP could be responsible, at least partially, in the lung alterations observed in welders.MethodsA combination of imaging and material science techniques including ((scanning) transmission electron microscopy ((S)TEM), energy dispersive X-ray (EDX), and X-ray microfluorescence (μXRF)), was used to characterize NP content in lung tissue from 21 welders and 21 matched control patients. Representative NP were synthesized, and their effects on macrophage inflammatory secretome and migration were evaluated, together with the effect of this macrophage inflammatory secretome on human lung primary fibroblasts differentiation.ResultsWelding-related NP (Fe, Mn, Cr oxides essentially) were identified in lung tissue sections from welders, in macrophages present in the alveolar lumen and in fibrous regions. In vitro macrophage exposure to representative NP (Fe2O3, Fe3O4, MnFe2O4 and CrOOH) induced the production of a pro-inflammatory secretome (increased production of CXCL-8, IL-1ß, TNF-α, CCL-2, −3, −4, and to a lesser extent IL-6, CCL-7 and −22), and all but Fe3O4 NP induce an increased migration of macrophages (Boyden chamber). There was no effect of NP-exposed macrophage secretome on human primary lung fibroblasts differentiation.ConclusionsAltogether, the data reported here strongly suggest that welding-related NP could be responsible, at least in part, for the pulmonary inflammation observed in welders. These results provide therefore the first evidence of a link between human exposure to NP and long-term pulmonary effects.
    Particle and Fibre Toxicology 05/2014; 11(1):23. DOI:10.1186/1743-8977-11-23 · 6.99 Impact Factor
  • Revue des Maladies Respiratoires 01/2014; 31:A194-A195. DOI:10.1016/j.rmr.2013.10.128 · 0.49 Impact Factor
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    ABSTRACT: Abstract Engineered nanoparticles are increasingly used in medical applications and day-to-day consumer products, leading to concerns about the potential environmental and human health impacts. Silver nanoparticles are particularly prevalent because of their use as anti-bacterial agents in many commonly available products. Nanoparticles (NPs) are believed to accumulate, often preferentially, in the liver. This study therefore investigates the effect of a silver NP (20 nm) on the liver, and in particular, the role of Kupffer cells (KCs; resident liver macrophages) in the overall inflammatory response in the organ. Cytokine expression in the normal liver was measured in terms of IL2, IL4, TNF-α, IFN-γ and IL10 released from the organ with significant up-regulation of TNF-α and IL10 being observed. For livers in which the KC population was specifically targeted and destroyed this cytokine increase was significantly decreased in comparison to the normal tissue. IL10 was secreted at approximately three times the concentration of TNF-α in all the test cases. The high levels of IL10 released from the normal tissue in comparison to the KC depleted livers suggest that the cytokine may help to protect against a pro-inflammatory response to these Ag NPs. This may indicate a potentially important role for KCs in the anti-inflammatory response and suggests that tolerance to the Ag NPs is favoured over a fully activated immune response. In addition, albumin production was measured as an indicator of hepatic function. It was noted that the liver function was unaffected by the Ag NPs.
    Nanotoxicology 12/2013; DOI:10.3109/17435390.2013.866284 · 7.34 Impact Factor
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    ABSTRACT: Carbon monoxide-releasing molecules (CORMs) represent a pharmacological alternative to CO gas inhalation. Here, we questioned whether CORM-3, a well-characterized water-soluble CORM, could prevent and reverse pulmonary hypertension (PH) in chronically hypoxic mice and in smooth muscle promoter 22 serotonin transporter mice overexpressing the serotonin transporter in smooth muscle cells (SMCs). Treatment with CORM-3 (50 mg/kg per day once daily) for 3 weeks prevented PH, right ventricular hypertrophy, and distal pulmonary artery muscularization in mice exposed to chronic hypoxia and partially reversed PH in smooth muscle promoter 22 serotonin transporter mice by reducing Ki67 dividing pulmonary artery SMCs (PA-SMCs). In these models, CORM-3 markedly increased lung p21 mRNA and protein levels and p21-stained PA-SMCs. These effects contrasted with the transient pulmonary vasodilatation and rise in lung cGMP levels induced by a single injection of CORM-3 in mice exposed to acute hypoxia. Studies in cultured rat PA-SMCs revealed that the inhibitory effects of CORM-3 on cell growth were independent of cGMP formation but associated with increased p21 mRNA and protein levels. Protection against PH by CORM-3 required increased lung expression of p21, as indicated by the inability of CORM-3 to prevent chronic hypoxia-induced PH in p21-deficient mice and to alter the growth of PA-SMCs derived from p21-deficient mice. CORM-3-induced p21 overexpression was linked to p53 activation as assessed by the inability of CORM-3 to prevent PH and induce p21 expression in p53-deficient mice and in PA-SMCs derived from p53-deficient mice. CORM-3 inhibits pulmonary vascular remodeling via p21, which may represent a useful approach for treating PH.
    Arteriosclerosis Thrombosis and Vascular Biology 12/2013; 34(2). DOI:10.1161/ATVBAHA.113.302302 · 5.53 Impact Factor
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    ABSTRACT: In the last few years questions have been raised regarding the potential toxicity of carbon nanotubes (CNT) to human and environment. It is believed that the physico-chemical characteristics of these materials are key determinants of CNT interaction with living organisms, and hence determine their toxicity. As for other nanomaterials, the most important of these characteristics are the length, diameter, surface area, tendency to agglomerate, bio-durability, presence and nature of catalyst residues as well as chemical functionalization of the CNT. This review highlights the recent advancements in the understanding of the CNT properties which are essential in determining CNT toxicity. Hence the focus is on CNT dimensions, surface properties, bio-durability and corona formation as these fields have evolved greatly in recent years. A deeper understanding of these events and their underlying mechanisms could provide a molecular explanation of the biological and physiological responses following CNT administration and therefore help in the development of safe by design materials.
    Advanced drug delivery reviews 08/2013; DOI:10.1016/j.addr.2013.07.019 · 12.71 Impact Factor
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    ABSTRACT: Carbon nanotubes (CNT) are a family of materials featuring a large range of length, diameter, numbers of walls and, quite often metallic impurities coming from the catalyst used for their synthesis. They exhibit unique physical properties, which have already led to an extensive development of CNT for numerous applications. Because of this development and the resulting potential increase of human exposure, an important body of literature has been published with the aim to evaluate the health impact of CNT. However, despite evidences of uptake and long-term persistence of CNT within macrophages and the central role of those cells in the CNT-induced pulmonary inflammatory response, a limited amount of data is available so far on the CNT fate inside macrophages. Therefore, the overall aim of our study was to investigate the fate of pristine single walled CNT (SWCNT) after their internalization by macrophages. To achieve our aim, we used a broad range of techniques that aimed at getting a comprehensive characterization of the SWCNT and their catalyst residues before and after exposure of murine macrophages: X-ray diffraction (XRD), High Resolution (HR) Transmission Electron Microscopy (TEM), High Angle Annular Dark Field-Scanning TEM (HAADF-STEM) coupled to Electron Energy Loss Spectroscopy (EELS), as well as micro-X-ray fluorescence mapping (muXRF), using synchrotron radiation. We showed 1) the rapid detachment of part of the iron nanoparticles initially attached to SWCNT which appeared as free iron nanoparticles in the cytoplasm and nucleus of CNT-exposed murine macrophages, and 2) that blockade of intracellular lysosomal acidification prevented iron nanoparticles detachment from CNT bundles and protected cells from CNT downstream toxicity. The present results, while obtained with pristine SWCNT, could likely be extended to other catalyst-containing nanomaterials and surely open new ways in the interpretation and understanding of CNT toxicity.
    Particle and Fibre Toxicology 06/2013; 10(1):24. DOI:10.1186/1743-8977-10-24 · 6.99 Impact Factor
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    ABSTRACT: ABSTRACT The mucociliary system, consisting of mucus-secreting goblet cells and ciliated cells, generates a constant overturning layer of protective mucus that lines the airway epithelium. Mucus hypersecretion and the pathophysiological changes associated are hallmarks of many pulmonary diseases including asthma, chronic obstructive pulmonary disease, and cystic fibrosis. Excessive mucus production leads to airway obstruction and, because there is currently no effective treatment, contributes to morbidity and mortality of many patients. Goblet cell differentiation and mucus production are subject to extensive control. An emerging concept is that not all goblet cells are phenotypically identical suggesting that specific molecular pathways orchestrate mucin overproduction. This paper attempts to describe the cellular and molecular mechanisms governing the differentiation of goblet cells in pulmonary diseases, a prerequisite for the development of new therapeutic agents.
    Experimental Lung Research 05/2013; DOI:10.3109/01902148.2013.791733 · 1.75 Impact Factor
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    ABSTRACT: Aims: Heme oxygenase-1 (HO-1, HMOX1) can prevent tumor initiation while in various tumors it has been demonstrated to promote growth, angiogenesis and metastasis. Here we investigated whether HMOX1 can modulate microRNAs and regulate human non-small cell lung cancer (NSCLC) development. Results: Stable HMOX1 overexpression in NSCLC NCI-H292 cells upregulated tumor suppressive microRNAs, whereas significantly diminished expression of oncomirs and angiomirs. The most potently downregulated was miR-378. HMOX1 also upregulated p53, downregulated Ang-1 and MUC5AC, reduced proliferation, migration and diminished angiogenic potential. Carbon monoxide was a mediator of HMOX1 effects on proliferation, migration and miR-378 expression. In contrast, stable miR-378 overexpression decreased HMOX1 and p53, while enhanced expression of MUC5AC, VEGF, IL-8 and Ang-1 and consequently increased proliferation, migration and stimulation of endothelial cells. Adenoviral delivery of HMOX1 reversed miR-378 effect on proliferation and migration of cancer cells. In vivo, HMOX1 overexpressing tumors were smaller, less vascularized and oxygenated and less metastatic. Overexpression of miR-378 exerted opposite effects. Accordingly, in patients with NSCLC, HMOX1 expression was lower in metastases to lymph nodes than in primary tumors. Innovation and Conclusion: In vitro and in vivo data indicate that the interplay between HMOX1 and miR-378 significantly modulates NSCLC progression and angiogenesis, suggesting miR-378 as a new therapeutic target. Rebound Track: This work was rejected during standard peer review and rescued by Rebound Peer Review (Antoxid Redox Signal 16: 293-296, 2012) with the following serving as open reviewers: James F. George, Mahin D. Maines, Justin C. Mason and Yasufumi Sato.
    Antioxidants & Redox Signaling 04/2013; DOI:10.1089/ars.2013.5184 · 7.67 Impact Factor
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    ABSTRACT: BACKGROUND: Induction of cellular senescence through activation of the p53 tumor suppressor protein is a new option for treating proliferative disorders. Nutlins prevent the ubiquitin ligase MDM2 (murine double minute 2), a negative p53 regulator, from interacting with p53. We hypothesized that cell senescence induced by Nutlin-3a exerted therapeutic effects in pulmonary hypertension (PH) by limiting the proliferation of pulmonary-artery smooth muscle cells (PA-SMCs). METHODS AND RESULTS: Nutlin-3a treatment of cultured human PA-SMCs resulted in cell growth arrest with the induction of senescence but not apoptosis; increased phosphorylated p53 protein levels; and expression of p53 target genes including p21, Bax, BTG2, and MDM2. Daily intraperitoneal Nutlin-3a treatment for 3 weeks dose-dependently reduced PH, right ventricular hypertrophy, and distal pulmonary artery muscularization in mice exposed to chronic hypoxia or SU5416/hypoxia. Nutlin-3a treatment also partially reversed PH in chronically hypoxic or transgenic mice overexpressing the serotonin-transporter in SMCs (SM22-5HTT+ mice). In these mouse models of PH, Nutlin-3a markedly increased senescent p21-stained PA-SMCs; lung p53, p21, and MDM2 protein levels; and p21, Bax, PUMA, BTG2, and MDM2 mRNA levels; but induced only minor changes in control mice without PH. Marked MDM2 immunostaining was seen in both mouse and human remodeled pulmonary vessels, supporting the use of Nutlins as a PH-targeted therapy. PH prevention or reversal by Nutlin-3a required lung p53 stabilization and increased p21 expression, as indicated by the absence of Nutlin-3a effects in hypoxia-exposed p53(-/-) and p21(-/-) mice. CONCLUSIONS: Nutlin-3a may hold promise as a prosenescence treatment targeting PA-SMCs in PH.
    Circulation 03/2013; 127(16). DOI:10.1161/CIRCULATIONAHA.113.002434 · 14.95 Impact Factor
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    ABSTRACT: Rationale. Chronic obstructive pulmonary disease (COPD) is associated with lung fibroblast senescence, a process characterized by the irreversible loss of replicative capacity associated with the secretion of inflammatory mediators. However, the mechanisms of this phenomenon remain poorly defined. Objectives. The aim of this study was to analyze the role of prostaglandin E2 (PGE2), a prostaglandin known to be increased in COPD lung fibroblasts, in inducing senescence and related inflammation in vitro in lung fibroblasts and in vivo in mice. Methods and main results. Lung fibroblasts from COPD patients exhibited higher expression of PGE2 receptors EP2 and EP4 as compared to non-smoker and smoker controls. Compared to both non-smoker and smoker controls, during long-term culture, COPD fibroblasts displayed increased senescent markers (increased senescence associated-β galactosidase activity, p16 and p53 expression and lower proliferative capacity), and an increased PGE2, IL6, IL8, GRO, CX3CL1 and MMP2 protein and COX2 and mPGES-1 mRNA expression. Using in vitro pharmacological approaches and in vivo experiments in wild type and p53 -/- mice we demonstrated that PGE2 produced by senescent COPD fibroblasts is responsible of the increased senescence and related inflammation. PGE2 acts either paracrinally or autocrinally via a pathway involving EP2 and EP4 prostaglandin receptors, COX2-dependent reactive oxygen species production and signaling, and consecutive p53 activation. Conclusion. PGE2 is a critical component of an amplifying and self-perpetuating circle inducing senescence and inflammation in COPD fibroblasts. Modulating the described PGE2 signaling pathway could provide new basis to dampen senescence and senescence-associated inflammation in COPD.
    American Journal of Respiratory and Critical Care Medicine 01/2013; 187(7). DOI:10.1164/rccm.201208-1361OC · 11.99 Impact Factor
  • Revue des Maladies Respiratoires 01/2013; 30:A10. DOI:10.1016/j.rmr.2012.10.037 · 0.49 Impact Factor

Publication Stats

4k Citations
778.68 Total Impact Points


  • 2009–2015
    • Université Paris-Est Créteil Val de Marne - Université Paris 12
      • Faculty of medicine
      Créteil, Île-de-France, France
    • Institut national de l'environnement industriel et des risques
      Verneuil, Picardie, France
  • 2008–2015
    • University of Paris-Est
      La Haye-Descartes, Centre, France
  • 1994–2013
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 1992–2012
    • French Institute of Health and Medical Research
      • Mondor Institute for Biomedical Research
      Lutetia Parisorum, Île-de-France, France
  • 2011
    • Centre Hospitalier Intercommunal Creteil
      Créteil, Île-de-France, France
  • 2006–2010
    • Assistance Publique – Hôpitaux de Paris
      Lutetia Parisorum, Île-de-France, France
    • Cheikh Anta Diop University, Dakar
      Dakar, Dakar, Senegal
  • 2007–2009
    • Paris Diderot University
      Lutetia Parisorum, Île-de-France, France
    • Harvard University
      • Department of Molecular and Cell Biology
      Cambridge, Massachusetts, United States
  • 2007–2008
    • Jagiellonian University
      • • Faculty of Biochemistry, Biophysics and Biotechnology
      • • Department of Medical Biotechnology
      Cracovia, Lesser Poland Voivodeship, Poland
  • 2006–2008
    • Hôpital Bichat - Claude-Bernard (Hôpitaux Universitaires Paris Nord Val de Seine)
      Lutetia Parisorum, Île-de-France, France
  • 1999
    • University of Buenos Aires
      Buenos Aires, Buenos Aires F.D., Argentina