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1. Evidence That SARS-CoV-2 Induces Lung Cell Senescence: Potential Impact on COVID-19 Lung Disease

Author

Emmanuelle Born, Jean-Michel Flaman, Charles Fouillade, Roger Le Grand, Larissa Lipskaia, Serge Adnot, Quentin Pascal, Arturo London-Vallejo, David Bernard, Pauline Maisonnasse, Valentin Sencio, François Trottein, Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Immunologie des maladies virales, auto-immunes, hématologiques et bactériennes (IMVA-HB), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Dynamique de l'information génétique : bases fondamentales et cancer (DIG CANCER), Centre National de la Recherche Scientifique (CNRS)-Institut Curie [Paris]-Sorbonne Université (SU), Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 (CIIL), Centre National de la Recherche Scientifique (CNRS)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université de Lille-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Protéomique, Réponse Inflammatoire, Spectrométrie de Masse (PRISM) - U 1192 (PRISM), Université de Lille-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut des Maladies Emergentes et des Thérapies Innovantes (IMETI), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, ATMEL [Rousset], CHU Henri Mondor, Supported by grants from the ANR AAP Flash COVID19 under reference AM-CoV-Path (RLG), ANR AAP Recherche-Action COVID19 under reference SENOCOVID - ANR 20 COV3 0006, ANR (Lustra), ANR (Influenzaging), the Institut National Du Cancer (INCA), EDF (CT9818), the Fondation pour la Recherche Médicale (FRM), and La Ligue contre le Cancer-Paris (RS21/75-24)., ANR-20-COVI-0021,AM-Cov-Path,Pathogénèse de l'infection SARS-Cov-2 dans un modèle de primates non humains : un modèle pour les traitements et la prévention(2020), ANR-20-COV3-0006,SENOCOVID,La sénescence cellulaire pulmonaire comme cible pour contrôler le COVID-19(2020), ANR-19-CE14-0015,Lustra,Fibrogenèse pulmonaire: approche systémique par transcriptomique spatiale(2019), ANR-20-CE14-0023,INFLUENZAGING,La sénescence cellulaire pulmonaire induite par le virus influenza: déterminant de la sévérité de l'atteinte respiratoire et de l'induction des maladies pulmonaires chroniques(2020), Institut Curie [Paris]-Sorbonne Université (SU)-Centre National de la Recherche Scientifique (CNRS), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Gestionnaire, HAL Sorbonne Université 5, Pathogénèse de l'infection SARS-Cov-2 dans un modèle de primates non humains : un modèle pour les traitements et la prévention - - AM-Cov-Path2020 - ANR-20-COVI-0021 - COVID-19 - VALID, La sénescence cellulaire pulmonaire comme cible pour contrôler le COVID-19 - - SENOCOVID2020 - ANR-20-COV3-0006 - COVID-19 - VALID, Fibrogenèse pulmonaire: approche systémique par transcriptomique spatiale - - Lustra2019 - ANR-19-CE14-0015 - AAPG2019 - VALID, La sénescence cellulaire pulmonaire induite par le virus influenza: déterminant de la sévérité de l'atteinte respiratoire et de l'induction des maladies pulmonaires chroniques - - INFLUENZAGING2020 - ANR-20-CE14-0023 - AAPG2020 - VALID, and CHU Henri Mondor [Créteil]

Subjects
Lung Diseases, Pulmonary and Respiratory Medicine, Senescence, 2019-20 coronavirus outbreak, Coronavirus disease 2019 (COVID-19), Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Clinical Biochemistry, Cell, [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], Biology, 03 medical and health sciences, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, medicine, Animals, Humans, Lung, Molecular Biology, Cellular Senescence, ComputingMilieux_MISCELLANEOUS, 030304 developmental biology, [SDV.MP.VIR] Life Sciences [q-bio]/Microbiology and Parasitology/Virology, 0303 health sciences, Potential impact, SARS-CoV-2, COVID-19, Cell Biology, Virology, 3. Good health, Macaca fascicularis, medicine.anatomical_structure, 030228 respiratory system, Lung disease, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, [SDV.IMM]Life Sciences [q-bio]/Immunology
Abstract

International audience

Published
2022

2. Eliminating senescent cells can promote pulmonary hypertension development and progression

Author

Emmanuelle Born, Larissa Lipskaia, Marielle Breau, Amal Houssaini, Delphine Beaulieu, Elisabeth Marcos, Remi Pierre, Marcio Do Cruzeiro, Marine Lefevre, Genevieve Derumeaux, Dmitry V. Bulavin, Marion Delcroix, Rozenn Quarck, Virinder Reen, Jesus Gil, David Bernard, Jean-Michel Flaman, Serge Adnot, and Shariq Abid

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Background: Senescent cells (SCs) are involved in proliferative disorders, but their role in pulmonary hypertension remains undefined. We investigated SCs in patients with pulmonary arterial hypertension and the role of SCs in animal pulmonary hypertension models. Methods: We investigated senescence (p16, p21) and DNA damage (γ-H2AX, 53BP1) markers in patients with pulmonary arterial hypertension and murine models. We monitored p16 activation by luminescence imaging in p16-luciferase (p16 LUC/+ ) knock-in mice. SC clearance was obtained by a suicide gene (p16 promoter–driven killer gene construct in p16-ATTAC mice), senolytic drugs (ABT263 and cell-permeable FOXO4-p53 interfering peptide [FOXO4-DRI]), and p16 inactivation in p16 LUC/LUC mice. We investigated pulmonary hypertension in mice exposed to normoxia, chronic hypoxia, or hypoxia+Sugen, mice overexpressing the serotonin transporter (SM22-5-HTT + ), and rats given monocrotaline. Results: Patients with pulmonary arterial hypertension compared with controls exhibited high lung p16, p21, and γ-H2AX protein levels, with abundant vascular cells costained for p16, γ-H2AX, and 53BP1. Hypoxia increased thoracic bioluminescence in p16 LUC/+ mice. In wild-type mice, hypoxia increased lung levels of senescence and DNA-damage markers, senescence-associated secretory phenotype components, and p16 staining of pulmonary endothelial cells (P-ECs, 30% of lung SCs in normoxia), and pulmonary artery smooth muscle cells. SC elimination by suicide gene or ABT263 increased the right ventricular systolic pressure and hypertrophy index, increased vessel remodeling (higher dividing proliferating cell nuclear antigen–stained vascular cell counts during both normoxia and hypoxia), and markedly decreased lung P-ECs. Pulmonary hemodynamic alterations and lung P-EC loss occurred in older p16 LUC/LUC mice, wild-type mice exposed to Sugen or hypoxia+Sugen, and SM22-5-HTT + mice given either ABT263 or FOXO4-DRI, compared with relevant controls. The severity of monocrotaline-induced pulmonary hypertension in rats was decreased slightly by ABT263 for 1 week but was aggravated at 3 weeks, with loss of P-ECs. Conclusions: Elimination of senescent P-ECs by senolytic interventions may worsen pulmonary hemodynamics. These results invite consideration of the potential impact on pulmonary vessels of strategies aimed at controlling cell senescence in various contexts.

Published
2022

3. Contributors

Author

Shariq Abid, Serge Adnot, Alvar Agusti, Delphine Beaulieu, Anil Bhushan, Thomas G. Bird, Emmanuelle Born, Marielle Breau, Alexander F. Chin, Jennifer H. Elisseeff, Zulrahman Erlangga, Konstantinos Evangelou, Rosa Faner, Joshua N. Farr, Eleni Georgakopoulou, Estela González-Gualda, Vassilis G. Gorgoulis, Elise Gray-Gaillard, Jin Han, Fernanda Hernandez-Gonzalez, Amal Houssaini, Michael D. Jensen, Diana Jurk, Goro Katsuumi, Sundeep Khosla, Christos Kiourtis, James L. Kirkland, Marta Kovatcheva, Larissa Lipskaia, Jose Alberto López-Domínguez, David Macías, Elisabeth Marcos, Mate Maus, Anette Melk, Kathleen Meyer, John Michel, Tohru Minamino, Satomi Miwa, David G. Monroe, Daniel Muñoz-Espín, Hui-Ling Ou, Allyson K. Palmer, Nayuta Saito, Roland Schmitt, Jacobo Sellares, Manuel Serrano, Myong-Hee Sung, Tamara Tchkonia, Peter J. Thompson, Thomas von Zglinicki, Tengfei Wan, and Peisu Zhang

Published
2022

4. Phospholipase A2 receptor 1 promotes lung cell senescence and emphysema in obstructive lung disease

Author

Shariq Abid, Marine Lefevre, David Bernard, Serge Adnot, Marielle Breau, Geneviève Derumeaux, Hiba Noureddine, Nora Vienney, Aya Attwe, Delphine Goehrig, Larissa Lipskaia, D. Beaulieu, Sara Jaber, Philippe Bertolino, Bernard Maitre, Emmanuelle Born, Elisabeth Marcos, Jin Huang, David Vindrieux, Amal Houssaini, Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Université Libanaise, Institut Mutualiste de Montsouris (IMM), Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Bernard, David, and Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)

Subjects
Pulmonary and Respiratory Medicine, Senescence, Ruxolitinib, [SDV]Life Sciences [q-bio], Mice, Pulmonary Disease, Chronic Obstructive, 03 medical and health sciences, 0302 clinical medicine, Fibrosis, medicine, Animals, Humans, Lung emphysema, 030212 general & internal medicine, Lung, Cellular Senescence, Emphysema, COPD, business.industry, Receptors, Phospholipase A2, respiratory system, medicine.disease, Pulmonary hypertension, Obstructive lung disease, 3. Good health, respiratory tract diseases, [SDV] Life Sciences [q-bio], medicine.anatomical_structure, Pulmonary Emphysema, 030228 respiratory system, Cancer research, business, medicine.drug
Abstract

BackgroundCell senescence is a key process in age-associated dysfunction and diseases, notably chronic obstructive pulmonary disease (COPD). We previously identified phospholipase A2 receptor 1 (PLA2R1) as a positive regulator of cell senescence acting via Janus kinase (JAK)/signal transducer and activator of transcription (STAT) signalling. Its role in pathology, however, remains unknown. Here, we assessed PLA2R1-induced senescence in COPD and lung emphysema pathogenesis.MethodsWe assessed cell senescence in lungs and cultured lung cells from patients with COPD and controls subjected to PLA2R1 knockdown, PLA2R1 gene transduction and treatment with the JAK1/2 inhibitor ruxolitinib. To assess whether PLA2R1 upregulation caused lung lesions, we developed transgenic mice overexpressing PLA2R1 (PLA2R1-TG) and intratracheally injected wild-type mice with a lentiviral vector carrying the Pla2r1 gene (LV-PLA2R1 mice).ResultsWe found that PLA2R1 was overexpressed in various cell types exhibiting senescence characteristics in COPD lungs. PLA2R1 knockdown extended the population doubling capacity of these cells and inhibited their pro-inflammatory senescence-associated secretory phenotype (SASP). PLA2R1-mediated cell senescence in COPD was largely reversed by treatment with the potent JAK1/2 inhibitor ruxolitinib. Five-month-old PLA2R1-TG mice exhibited lung cell senescence, and developed lung emphysema and lung fibrosis together with pulmonary hypertension. Treatment with ruxolitinib induced reversal of lung emphysema and fibrosis. LV-PLA2R1-treated mice developed lung emphysema within 4 weeks and this was markedly attenuated by concomitant ruxolitinib treatment.ConclusionsOur data support a major role for PLA2R1 activation in driving lung cell senescence and lung alterations in COPD. Targeting JAK1/2 may represent a promising therapeutic approach for COPD.

Published
2021

5. The antioxidant N-acetylcysteine protects from lung emphysema but induces lung adenocarcinoma in mice

Author

Jean-Michel Flaman, Shariq Abid, Marielle Breau, David Bernard, Serge Adnot, D. Beaulieu, Alberta Palazzo, Aya Attwe, Brigitte Bourachot, Amal Houssaini, Jeanne Tran Van Nhieu, Emmanuelle Born, Larissa Lipskaia, Gabor Czibik, Guillaume Collin, Elisabeth Marcos, Fatima Mechta-Grigoriou, Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Physiopathologie, génétique et pharmacologie du remodelage cardiovasculaire, Université Pierre et Marie Curie - Paris 6 (UPMC)-IFR14-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherche en Cancérologie de Lyon (CRCL), Centre Léon Bérard [Lyon]-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de recherches de biochimie macromoléculaire (CRBM), Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-IFR122-Centre National de la Recherche Scientifique (CNRS), Département de pathologie [Mondor], Assistance publique - Hôpitaux de Paris (AP-HP) (APHP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), CEA Cadarache, Commissariat à l'énergie atomique et aux énergies alternatives (CEA), Transduction du signal et oncogénèse, Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Curie, Faculté de Médecine Créteil, Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), INSERM U955, équipe 8, Hypertension arterielle pulmonaire physiopathologie et innovation thérapeutique, Centre chirurgical Marie Lannelongue-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre chirurgical Marie Lannelongue-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-IFR10, Centre de Recherche en Cancérologie de Lyon (UNICANCER/CRCL), Centre de recherche en Biologie Cellulaire (CRBM), Université Montpellier 1 (UM1)-Université Montpellier 2 - Sciences et Techniques (UM2)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Henri Mondor-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre chirurgical Marie Lannelongue-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre chirurgical Marie Lannelongue, Centre de recherche en Biologie cellulaire de Montpellier (CRBM), and Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS)

Subjects
Lung Diseases, Male, 0301 basic medicine, Lung Neoplasms, Pulmonology, Proto-Oncogene Proteins c-jun, [SDV]Life Sciences [q-bio], [SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC], medicine.disease_cause, Antioxidants, Acetylcysteine, Mice, 0302 clinical medicine, Lung emphysema, Lung, ComputingMilieux_MISCELLANEOUS, Cancer, Mice, Knockout, COPD, General Medicine, respiratory system, 3. Good health, medicine.anatomical_structure, Pulmonary Emphysema, Oncology, 030220 oncology & carcinogenesis, Female, Lung cancer, Research Article, medicine.drug, Senescence, Adenocarcinoma of Lung, 03 medical and health sciences, medicine, Animals, Humans, business.industry, medicine.disease, respiratory tract diseases, Disease Models, Animal, Oxidative Stress, 030104 developmental biology, Cancer research, Reactive Oxygen Species, business, Oxidative stress
Abstract

International audience; Oxidative stress is a major contributor to chronic lung diseases. Antioxidants such as N-acetylcysteine (NAC) are broadly viewed as protective molecules that prevent the mutagenic effects of reactive oxygen species. Antioxidants may, however, increase the risk of some forms of cancer and accelerate lung cancer progression in murine models. Here, we investigated chronic NAC treatment in aging mice displaying lung oxidative stress and cell senescence due to inactivation of the transcription factor JunD, which is downregulated in diseased human lungs. NAC treatment decreased lung oxidative damage and cell senescence and protected from lung emphysema but concomitantly induced the development of lung adenocarcinoma in 50% of JunD-deficient mice and 10% of aged control mice. This finding constitutes the first evidence to our knowledge of a carcinogenic effect of antioxidant therapy in the lungs of aged mice with chronic lung oxidative stress and warrants the utmost caution when considering the therapeutic use of antioxidants.

Published
2019

7. Phospholipase A2 Receptor 1 Promotes Lung-Cell Senescence and Emphysema in Obstructive Lung Disease

Author

Serge Adnot, Elisabeth Marcos, Shariq Abid, Bernard Maitre, David Bernard, Amal Houssaini, David Vindrieux, Larissa Lipskaia, D. Beaulieu, Marielle Breau, Jin Huang, Emmanuelle Born, Nora Vienney, and Aya Attwe

Subjects
Senescence, Lung, medicine.anatomical_structure, business.industry, Cell, medicine, Cancer research, medicine.disease, business, Obstructive lung disease, Phospholipase A2 receptor
Published
2019

8. Chronic Antioxidant NAcetylcysteine Treatment Induces Lung Cancer Formation in Mice

Author

Elisabeth Marcos, Fatima Mechta-Grigoriou, Amal Houssaini, G. Collin, Gabor Czibik, S. Abid, A. Pallazo, A. Attwe, Marielle Breau, Brigitte Bourachot, D. Beaulieu, David Bernard, Larissa Lipskaia, S. Adnot, and Emmanuelle Born

Subjects
Antioxidant, business.industry, medicine.medical_treatment, Cancer research, Medicine, business, Lung cancer, medicine.disease
Published
2019

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