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425 results on '"Boucherat, Olivier"'

1. Seeing pulmonary hypertension through a paediatric lens: a viewpoint.

Author

Agarwal, Stuti, Fineman, Jeffrey, Cornfield, David, Alvira, Cristina, Zamanian, Roham, Goss, Kara, Yuan, Ke, Bonnet, Sebastien, Boucherat, Olivier, Pullamsetti, Soni, Alcázar, Miguel, Goncharova, Elena, Kudryashova, Tatiana, Nicolls, Mark, and de Jesús Pérez, Vinicio

Subjects
Humans, Hypertension, Pulmonary, Child, Pediatrics
Abstract

Paediatric pulmonary hypertension (PH) offers unique genetic and developmental insights that can help in the discovery of novel mechanisms and targets to treat adult PH https://bit.ly/3TMm6bi

Published
2024

2. Deficiency of the Deubiquitinase UCHL1 Attenuates Pulmonary Arterial Hypertension

Author

Tang, Haiyang, Gupta, Akash, Morrisroe, Seth A., Bao, Changlei, Schwantes-An, Tae-Hwi, Gupta, Geetanjali, Liang, Shuxin, Sun, Yanan, Chu, Aiai, Luo, Ang, Ramamoorthi Elangovan, Venkateswaran, Sangam, Shreya, Shi, Yinan, Naidu, Samisubbu R., Jheng, Jia-Rong, Ciftci-Yilmaz, Sultan, Warfel, Noel A., Hecker, Louise, Mitra, Sumegha, Coleman, Anna W., Lutz, Katie A., Pauciulo, Michael W., Lai, Yen-Chun, Javaheri, Ali, Dharmakumar, Rohan, Wu, Wen-Hui, Flaherty, Daniel P., Karnes, Jason H., Breuils-Bonnet, Sandra, Boucherat, Olivier, Bonnet, Sebastien, Yuan, Jason X.-J., Jacobson, Jeffrey R., Duarte, Julio D., Nichols, William C., Garcia, Joe G.N., and Desai, Ankit A.

Published
2024
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3. Transcriptional profiling unveils molecular subgroups of adaptive and maladaptive right ventricular remodeling in pulmonary hypertension

Author

Khassafi, Fatemeh, Chelladurai, Prakash, Valasarajan, Chanil, Nayakanti, Sreenath Reddy, Martineau, Sandra, Sommer, Natascha, Yokokawa, Tetsuro, Boucherat, Olivier, Kamal, Aryan, Kiely, David G., Swift, Andrew J., Alabed, Samer, Omura, Junichi, Breuils-Bonnet, Sandra, Kuenne, Carsten, Potus, Francois, Günther, Stefan, Savai, Rajkumar, Seeger, Werner, Looso, Mario, Lawrie, Allan, Zaugg, Judith B., Tello, Khodr, Provencher, Steeve, Bonnet, Sébastien, and Pullamsetti, Soni Savai

Published
2023
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4. Noncanonical HIPPO/MST Signaling via BUB3 and FOXO Drives Pulmonary Vascular Cell Growth and Survival

Author

Kudryashova, Tatiana V, Dabral, Swati, Nayakanti, Sreenath, Ray, Arnab, Goncharov, Dmitry A, Avolio, Theodore, Shen, Yuanjun, Rode, Analise, Pena, Andressa, Jiang, Lifeng, Lin, Derek, Baust, Jeffrey, Bachman, Timothy N, Graumann, Johannes, Ruppert, Clemens, Guenther, Andreas, Schmoranzer, Mario, Grobs, Yann, Lemay, Sarah Eve, Tremblay, Eve, Breuils-Bonnet, Sandra, Boucherat, Olivier, Mora, Ana L, DeLisser, Horace, Zhao, Jing, Zhao, Yutong, Bonnet, Sébastien, Seeger, Werner, Pullamsetti, Soni S, and Goncharova, Elena A

Subjects
Medical Physiology, Biomedical and Clinical Sciences, Lung, Rare Diseases, 2.1 Biological and endogenous factors, Aetiology, Cardiovascular, Animals, Cell Cycle Proteins, Cell Proliferation, Cells, Cultured, Chromosomal Proteins, Non-Histone, Forkhead Transcription Factors, Hypertension, Pulmonary, Hypoxia, Mammals, Mechanistic Target of Rapamycin Complex 1, Mice, Myocytes, Smooth Muscle, Poly-ADP-Ribose Binding Proteins, Proteomics, Proto-Oncogene Proteins c-akt, Pulmonary Arterial Hypertension, Pulmonary Artery, Vascular Remodeling, animals, hypoxia, mice, proteomic, pulmonary artery, Cardiorespiratory Medicine and Haematology, Clinical Sciences, Cardiovascular System & Hematology, Cardiovascular medicine and haematology, Clinical sciences
Abstract

RationaleThe MSTs (mammalian Ste20-like kinases) 1/2 are members of the HIPPO pathway that act as growth suppressors in adult proliferative diseases. Pulmonary arterial hypertension (PAH) manifests by increased proliferation and survival of pulmonary vascular cells in small PAs, pulmonary vascular remodeling, and the rise of pulmonary arterial pressure. The role of MST1/2 in PAH is currently unknown.ObjectiveTo investigate the roles and mechanisms of the action of MST1 and MST2 in PAH.Methods and resultsUsing early-passage pulmonary vascular cells from PAH and nondiseased lungs and mice with smooth muscle-specific tamoxifen-inducible Mst1/2 knockdown, we found that, in contrast to canonical antiproliferative/proapoptotic roles, MST1/2 act as proproliferative/prosurvival molecules in human PAH pulmonary arterial vascular smooth muscle cells and pulmonary arterial adventitial fibroblasts and support established pulmonary vascular remodeling and pulmonary hypertension in mice with SU5416/hypoxia-induced pulmonary hypertension. By using unbiased proteomic analysis, gain- and loss-of function approaches, and pharmacological inhibition of MST1/2 kinase activity by XMU-MP-1, we next evaluated mechanisms of regulation and function of MST1/2 in PAH pulmonary vascular cells. We found that, in PAH pulmonary arterial adventitial fibroblasts, the proproliferative function of MST1/2 is caused by IL-6-dependent MST1/2 overexpression, which induces PSMC6-dependent downregulation of forkhead homeobox type O 3 and hyperproliferation. In PAH pulmonary arterial vascular smooth muscle cells, MST1/2 acted via forming a disease-specific interaction with BUB3 and supported ECM (extracellular matrix)- and USP10-dependent BUB3 accumulation, upregulation of Akt-mTORC1, cell proliferation, and survival. Supporting our in vitro observations, smooth muscle-specific Mst1/2 knockdown halted upregulation of Akt-mTORC1 in small muscular PAs of mice with SU5416/hypoxia-induced pulmonary hypertension.ConclusionsTogether, this study describes a novel proproliferative/prosurvival role of MST1/2 in PAH pulmonary vasculature, provides a novel mechanistic link from MST1/2 via BUB3 and forkhead homeobox type O to the abnormal proliferation and survival of pulmonary arterial vascular smooth muscle cells and pulmonary arterial adventitial fibroblasts, remodeling and pulmonary hypertension, and suggests new target pathways for therapeutic intervention.

Published
2022

5. Defining the clinical validity of genes reported to cause pulmonary arterial hypertension

Author

Callejo, Emily P., Day, Kristina M., Macaya, Daniela, Maldonado-Velez, Gabriel, Archer, Stephen L., Auckland, Kathryn, Austin, Eric D., Badagliacca, Roberto, Barberà, Joan-Albert, Belge, Catharina, Bogaard, Harm Jan, Bonnet, Sébastien, Boomars, Karin A., Boucherat, Olivier, Chakinala, Murali M., Condliffe, Robin, Damico, Rachel Lynn, Delcroix, Marion, Desai, Ankit A., Doboszynska, Anna, Elliott, C. Greg, Eyries, Melanie, Escribano Subías, Maria Pilar, Gall, Henning, Ghio, Stefano, Ghofrani, Ardeschir-Hossein, Grünig, Ekkehard, Hamid, Rizwan, Harbaum, Lars, Hassoun, Paul M., Hemnes, Anna R., Hinderhofer, Katrin, Howard, Luke S., Humbert, Marc, Kiely, David G., Langleben, David, Lawrie, Allan, Loyd, Jim E., Moledina, Shahin, Montani, David, Morrell, Nichols W., Nichols, William C., Olschewski, Andrea, Olschewski, Horst, Papa, Silvia, Pauciulo, Mike W., Provencher, Steve, Quarck, Rozenn, Rhodes, Christopher J., Scelsi, Laura, Seeger, Werner, Stewart, Duncan J., Sweatt, Andrew, Swietlik, Emilia M., Treacy, Carmen, Trembath, Richard C., Tura-Ceide, Olga, Vizza, Carmine Dario, Vonk Noordegraaf, Anton, Wilkins, Martin R., Zamanian, Roham T., Zateyshchikov, Dmitry, Welch, Carrie L., Aldred, Micheala A., Balachandar, Srimmitha, Dooijes, Dennis, Eichstaedt, Christina A., Gräf, Stefan, Houweling, Arjan C., Machado, Rajiv D., Pandya, Divya, Prapa, Matina, Shaukat, Memoona, Southgate, Laura, Tenorio-Castano, Jair, and Chung, Wendy K.

Published
2023
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15. ATP Citrate Lyase Drives Vascular Remodeling Diseases Development Through Metabolic-Epigenetic Reprograming

Author

Grobs, Yann, primary, Romanet, Charlotte, additional, Lemay, Sarah-Eve, additional, Bourgeois, Alice, additional, Voisine, Pierre, additional, Theberge, Charlie, additional, Sauvaget, Melanie, additional, Breuils-Bonnet, Sandra, additional, Martineau, Sandra, additional, Kabbout, Reem El, additional, Mougin, Manon, additional, Dumais, Elizabeth, additional, Perron, Jean, additional, Flamand, Nicolas, additional, Potus, François, additional, Provencher, Steeve, additional, Boucherat, Olivier, additional, and Bonnet, Sebastien, additional

Published
2024
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16. Abstract 15564: Transcriptional Profiling Unveils New Molecular Subgroups of Adaptive and Maladaptive Right Ventricular Remodeling in Pulmonary Hypertension

Author

Khassafi, Fatemeh, Chelladurai, Prakash, Nayakanti, Sreenath R, Martineau, Sandra, Tello, Khodr, Sommer, Natascha, Omura, Junichi, Breuils Bonnet, Sandra, Kuenne, Carsten, Guenther, Stefan, potus, francois, Boucherat, Olivier, Provencher, Steeve, Savai, Rajkumar, Seeger, Werner, Looso, Mario, Bonnet, Sebastien, and Savai Pullamsetti, Soni

Published
2022
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18. Abstract 10904: Integrins Signaling Represents an Exciting Therapeutic Avenue to Counter Vascular Remodeling and Right Ventricular Failure in Pulmonary Arterial Hypertension

Author

Lemay, Sarah-Eve, Montesinos, Mónica S, Grobs, Yann, Yokokawa, Tetsuro, Shimauchi, Tsukasa, Breuils Bonnet, Sandra, Martineau, Sandra, SALEM, MABROUKA, Bourgeois, Alice, Romanet, Charlotte, HUANG, XINQIANG, Dowling, James, Lu, Min, Ray, Adrian, Potus, Francois, Provencher, Steeve, Boucherat, Olivier, and Bonnet, Sebastien

Published
2022
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21. Abstract 9929: Epigenome-Wide-Association-Study Characterizes DNA Methylation Changes Associated With Lung and Right Ventricle Dysfunction in Pulmonary Hypertension

Author

Potus, Francois, Azhar, Nabil, Reem, EL-Kabbout, Breuils Bonnet, Sandra, Martineau, Sandra, Krishna, Vinod, Kalyana-Sundaram, Shanker, Girard, Lysanne, Toro, Victoria M, Boucherat, Olivier, Guerra Bonilla, Fany, Gutstein, David, Provencher, Steeve, JEYASEELAN, Jey R, and Bonnet, Sebastien

Published
2022
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23. HDAC6: A Novel Histone Deacetylase Implicated in Pulmonary Arterial Hypertension

Author

Boucherat, Olivier, Chabot, Sophie, Paulin, Roxane, Trinh, Isabelle, Bourgeois, Alice, Potus, François, Lampron, Marie-Claude, Lambert, Caroline, Breuils-Bonnet, Sandra, Nadeau, Valérie, Paradis, Renée, Goncharova, Elena A, Provencher, Steeve, and Bonnet, Sébastien

Subjects
Rare Diseases, Cancer, Lung, 5.1 Pharmaceuticals, Aetiology, 2.1 Biological and endogenous factors, Development of treatments and therapeutic interventions, Cardiovascular, Acetylation, Animals, Apoptosis, Cell Line, Cell Movement, Cell Proliferation, Disease Models, Animal, Gene Expression, Gene Expression Regulation, HSP90 Heat-Shock Proteins, Histone Deacetylase 6, Histone Deacetylase Inhibitors, Humans, Hypertension, Pulmonary, Immunohistochemistry, Ku Autoantigen, Mice, Mice, Knockout, Models, Biological, Myocytes, Smooth Muscle, Rats, bcl-2-Associated X Protein
Abstract

Pulmonary arterial hypertension (PAH) is a vascular remodeling disease with limited therapeutic options. Although exposed to stressful conditions, pulmonary artery (PA) smooth muscle cells (PASMCs) exhibit a "cancer-like" pro-proliferative and anti-apoptotic phenotype. HDAC6 is a cytoplasmic histone deacetylase regulating multiple pro-survival mechanisms and overexpressed in response to stress in cancer cells. Due to the similarities between cancer and PAH, we hypothesized that HDAC6 expression is increased in PAH-PASMCs to face stress allowing them to survive and proliferate, thus contributing to vascular remodeling in PAH. We found that HDAC6 is significantly up-regulated in lungs, distal PAs, and isolated PASMCs from PAH patients and animal models. Inhibition of HDAC6 reduced PAH-PASMC proliferation and resistance to apoptosis in vitro sparing control cells. Mechanistically, we demonstrated that HDAC6 maintains Ku70 in a hypoacetylated state, blocking the translocation of Bax to mitochondria and preventing apoptosis. In vivo, pharmacological inhibition of HDAC6 improved established PAH in two experimental models and can be safely given in combination with currently approved PAH therapies. Moreover, Hdac6 deficient mice were partially protected against chronic hypoxia-induced pulmonary hypertension. Our study shows for the first time that HDAC6 is implicated in PAH development and represents a new promising target to improve PAH.

Published
2017

25. Hypusine Signaling Promotes Pulmonary Vascular Remodeling in Pulmonary Arterial Hypertension.

Author

Lemay, Sarah-Eve, Grobs, Yann, Romanet, Charlotte, Martineau, Sandra, Salem, Mabrouka, Shimauchi, Tsukasa, Breuils-Bonnet, Sandra, Bourgeois, Alice, Théberge, Charlie, Pelletier, Andréanne, Potus, François, Provencher, Steeve, Bonnet, Sébastien, and Boucherat, Olivier

Subjects
VASCULAR remodeling, PULMONARY arterial hypertension, POLYAMINES, POST-translational modification, LABORATORY rats, GENETIC translation
Abstract

Rationale: The ubiquitous polyamine spermidine is essential for cell survival and proliferation. One important function of spermidine is to serve as a substrate for hypusination, a posttranslational modification process that occurs exclusively on eukaryotic translation factor 5A (eIF5A) and ensures efficient translation of various gene products. Pulmonary arterial hypertension (PAH) is a life-threatening disease characterized by progressive obliteration of the small pulmonary arteries (PAs) caused by excessive proliferation of PA smooth muscle cells (PASMCs) and suppressed apoptosis. Objectives: To characterize the role of hypusine signaling in PAH. Methods: Molecular, genetic, and pharmacological approaches were used both in vitro and in vivo to investigate the role of hypusine signaling in pulmonary vascular remodeling. Measurements and Main Results: Hypusine forming enzymes—deoxyhypusine synthase (DHPS) and deoxyhypusine hydroxylase (DOHH)—and hypusinated eukaryotic translation factor 5A are overexpressed in distal PAs and isolated PASMCs from PAH patients and animal models. In vitro, inhibition of DHPS using N1-guanyl-1,7-diaminoheptane or shRNA resulted in a decrease in PAH-PASMC resistance to apoptosis and proliferation. In vivo, inactivation of one allele of Dhps targeted to smooth muscle cells alleviates PAH in mice, and its pharmacological inhibition significantly decreases pulmonary vascular remodeling and improves hemodynamics and cardiac function in two rat models of established PAH. With mass spectrometry, hypusine signaling is shown to promote the expression of a broad array of proteins involved in oxidative phosphorylation, thus supporting the bioenergetic requirements of cell survival and proliferation. Conclusions: These findings support inhibiting hypusine signaling as a potential treatment for PAH. [ABSTRACT FROM AUTHOR]

Published
2024
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27. Time Is Running Out in Pulmonary Arterial Hypertension: The Epigenetic Clock Is Clicking.

Author

El Kabbout, Reem, Azhar, Nabil, Breuils-Bonnet, Sandra, Krishna, Vinod, Kalyana-Sundaram, Shanker, Boucherat, Olivier, Provencher, Steeve, Bonnet, Sébastien, and Potus, François

Subjects
PULMONARY arterial hypertension, ENDOTHELIN receptors, MOLECULAR biology, EPIGENETICS, PULMONARY circulation, CYTOLOGY, KILLER cells
Abstract

The article focuses on pulmonary arterial hypertension (PAH), a condition characterized by increased pulmonary arterial pressure leading to right ventricular dysfunction and premature death. It explores the concept of biological aging acceleration in PAH, examining epigenetic age and age acceleration in various tissues/organs affected by the disease, suggesting a potential link between aging-related molecular dysfunctions and PAH progression.

Published
2024
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29. Identification of AURKB as a new actor in vascular remodeling in PAH

Author

Lemay, Sarah-Eve, primary, Sauvaget, Mélanie, additional, Mougin, Manon, additional, El Kabbout, Reem, additional, Martineau, Sandra, additional, Breuils-Bonnet, Sandra, additional, Bourgeois, Alice, additional, Salem, Mabrouka, additional, Théberge, Charlie, additional, Potus, François, additional, Provencher, Steeve, additional, Boucherat, Olivier, additional, and Bonnet, Sébastien, additional

Published
2023
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30. The Fibronectin-Binding Integrins System as a Contributor to PAH Pathogenesis

Author

Lemay, Sarah-Eve, primary, Montesinos, Mónica S, additional, Grobs, Yann, additional, Yokokawa, Tetsuro, additional, Shimauchi, Tsukasa, additional, Breuils-Bonnet, Sandra, additional, Martineau, Sandra, additional, Bourgeois, Alice, additional, Salem, Mabrouka, additional, Théberge, Charlie, additional, El Kabbout, Reem, additional, Romanet, Charlotte, additional, Lu, Min, additional, Huang, Xinqiang, additional, Dowling, James E, additional, Ray, Adrian S, additional, Potus, François, additional, Provencher, Steeve, additional, Boucherat, Olivier, additional, and Bonnet, Sébastien, additional

Published
2023
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32. Targeting ATP Citrate Lyase to mitigate Vascular Remodeling Pathogenesis.

Author

Grobs, Yann, primary, Romanet, Charlotte, additional, Bourgeois, Alice, additional, Lemay, Sarah-Eve, additional, Shimauchi, Tsukasa, additional, Breuils-Bonnet, Sandra, additional, Salem, Mabrouka, additional, Potus, Francois, additional, Provencher, Steeve, additional, Voisine, Pierre, additional, Boucherat, Olivier, additional, and Bonnet, Sebastien, additional

Published
2023
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34. Abstract 150: Targeting The Lipogenic Enzyme ATP Citrate Lyase As A Potential Therapy Against Coronary Artery Disease

Author

Grobs, Yann, primary, Lemay, Sarah-Eve S, additional, Romanet, Charlotte, additional, Bourgeois, Alice, additional, SALEM, MABROUKA, additional, Martineau, Sandra, additional, Breuils-Bonnet, Sandra, additional, Voisine, Pierre, additional, Potus, Francois, additional, Provencher, Steeve, additional, Boucherat, Olivier, additional, and Bonnet, Sebastien, additional

Published
2023
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48. G9a/GLP Targeting Ameliorates Pulmonary Vascular Remodeling in Pulmonary Arterial Hypertension

Author

Awada, Charifa, primary, Bourgeois, Alice, additional, Lemay, Sarah-Eve, additional, Grobs, Yann, additional, Yokokawa, Tetsuro, additional, Breuils-Bonnet, Sandra, additional, Martineau, Sandra, additional, Krishna, Vinod, additional, Potus, François, additional, Jeyaseelan, Jey, additional, Provencher, Steeve, additional, Bonnet, Sébastien, additional, and Boucherat, Olivier, additional

Published
2023
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49. Genetic counselling and testing in pulmonary arterial hypertension:a consensus statement on behalf of the International Consortium for Genetic Studies in PAH

Author

Eichstaedt, Christina A., Belge, Catharina, Chung, Wendy K., Gräf, Stefan, Grünig, Ekkehard, Montani, David, Quarck, Rozenn, Tenorio-Castano, Jair A., Soubrier, Florent, Trembath, Richard C., Morrell, Nicholas W., Aldred, Micheala A., Archer, Stephen L., Austin, Eric D., Badagliacca, Roberto, Balanchandar, Srimmitha, Barberà, Joan Albert, Benza, Raymond L., Berger, Rolf M.F., Bogaard, Harm Jan, Bonnet, Sébastien, Boomars, Karin A., Boucherat, Olivier, Chakinala, Murali M., Condliffe, Robin, Damico, Rachel Lynn, Delcroix, Marion, Desai, Ankit A., Doboszynska, Anna, Dooijes, Dennis, Elliott, C. Greg, Eyries, Melanie, Subías, Maria Pilar Escribano, Gall, Henning, García-Aranda, Beatriz, Ghio, Stefano, Ghofrani, Hossein Ardeschir, Hamid, Rizwan, Hassoun, Paul M., Hemnes, Anna R., Hinderhofer, Katrin, Houweling, Arjan C., Howard, Luke S., Humbert, Marc, Kiely, David G., Kovacs, Gabor, Langleben, David, Lapunzina, Pablo, Lawrie, Allan, Loyd, Jim E., Eichstaedt, Christina A., Belge, Catharina, Chung, Wendy K., Gräf, Stefan, Grünig, Ekkehard, Montani, David, Quarck, Rozenn, Tenorio-Castano, Jair A., Soubrier, Florent, Trembath, Richard C., Morrell, Nicholas W., Aldred, Micheala A., Archer, Stephen L., Austin, Eric D., Badagliacca, Roberto, Balanchandar, Srimmitha, Barberà, Joan Albert, Benza, Raymond L., Berger, Rolf M.F., Bogaard, Harm Jan, Bonnet, Sébastien, Boomars, Karin A., Boucherat, Olivier, Chakinala, Murali M., Condliffe, Robin, Damico, Rachel Lynn, Delcroix, Marion, Desai, Ankit A., Doboszynska, Anna, Dooijes, Dennis, Elliott, C. Greg, Eyries, Melanie, Subías, Maria Pilar Escribano, Gall, Henning, García-Aranda, Beatriz, Ghio, Stefano, Ghofrani, Hossein Ardeschir, Hamid, Rizwan, Hassoun, Paul M., Hemnes, Anna R., Hinderhofer, Katrin, Houweling, Arjan C., Howard, Luke S., Humbert, Marc, Kiely, David G., Kovacs, Gabor, Langleben, David, Lapunzina, Pablo, Lawrie, Allan, and Loyd, Jim E.

Abstract

Pulmonary arterial hypertension (PAH) is a rare disease that can be caused by (likely) pathogenic germline genomic variants. In addition to the most prevalent disease gene, BMPR2 (bone morphogenetic protein receptor 2), several genes, some belonging to distinct functional classes, are also now known to predispose to the development of PAH. As a consequence, specialist and non-specialist clinicians and healthcare professionals are increasingly faced with a range of questions regarding the need for, approaches to and benefits/risks of genetic testing for PAH patients and/or related family members. We provide a consensus-based approach to recommendations for genetic counselling and assessment of current best practice for disease gene testing. We provide a framework and the type of information to be provided to patients and relatives through the process of genetic counselling, and describe the presently known disease causal genes to be analysed. Benefits of including molecular genetic testing within the management protocol of patients with PAH include the identification of individuals misclassified by other diagnostic approaches, the optimisation of phenotypic characterisation for aggregation of outcome data, including in clinical trials, and importantly through cascade screening, the detection of healthy causal variant carriers, to whom regular assessment should be offered.

Published
2023

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