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Your search keyword '"Tatyana Novoyatleva"' showing total 6 results
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6 results on '"Tatyana Novoyatleva"'

1. C-type natriuretic peptide/cGMP/FoxO3 signaling attenuates hyperproliferation of pericytes from patients with pulmonary arterial hypertension

Author

Swati Dabral, Minhee Noh, Franziska Werner, Lisa Krebes, Katharina Völker, Christopher Maier, Ivan Aleksic, Tatyana Novoyatleva, Stefan Hadzic, Ralph Theo Schermuly, Vinicio A. de Jesus Perez, and Michaela Kuhn

Subjects
Biology (General), QH301-705.5
Abstract

Abstract Pericyte dysfunction, with excessive migration, hyperproliferation, and differentiation into smooth muscle-like cells contributes to vascular remodeling in Pulmonary Arterial Hypertension (PAH). Augmented expression and action of growth factors trigger these pathological changes. Endogenous factors opposing such alterations are barely known. Here, we examine whether and how the endothelial hormone C-type natriuretic peptide (CNP), signaling through the cyclic guanosine monophosphate (cGMP) -producing guanylyl cyclase B (GC-B) receptor, attenuates the pericyte dysfunction observed in PAH. The results demonstrate that CNP/GC-B/cGMP signaling is preserved in lung pericytes from patients with PAH and prevents their growth factor-induced proliferation, migration, and transdifferentiation. The anti-proliferative effect of CNP is mediated by cGMP-dependent protein kinase I and inhibition of the Phosphoinositide 3-kinase (PI3K)/AKT pathway, ultimately leading to the nuclear stabilization and activation of the Forkhead Box O 3 (FoxO3) transcription factor. Augmentation of the CNP/GC-B/cGMP/FoxO3 signaling pathway might be a target for novel therapeutics in the field of PAH.

Published
2024
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2. Author Correction: Deficiency of Axl aggravates pulmonary arterial hypertension via BMPR2

Author

Tatyana Novoyatleva, Nabham Rai, Baktybek Kojonazarov, Swathi Veeroju, Isabel Ben-Batalla, Paola Caruso, Mazen Shihan, Nadine Presser, Elsa Götz, Carina Lepper, Sebastian Herpel, Grégoire Manaud, Frédéric Perros, Henning Gall, Hossein Ardeschir Ghofrani, Norbert Weissmann, Friedrich Grimminger, John Wharton, Martin Wilkins, Paul D. Upton, Sonja Loges, Nicholas W. Morrell, Werner Seeger, and Ralph T. Schermuly

Subjects
Biology (General), QH301-705.5
Published
2022
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3. Correction to: Eplerenone attenuates pathological pulmonary vascular rather than right ventricular remodeling in pulmonary arterial hypertension

Author

Mario Boehm, Nadine Arnold, Adam Braithwaite, Josephine Pickworth, Changwu Lu, Tatyana Novoyatleva, David G. Kiely, Friedrich Grimminger, Hossein A. Ghofrani, Norbert Weissmann, Werner Seeger, Allan Lawrie, Ralph T. Schermuly, and Baktybek Kojonazarov

Subjects
Diseases of the respiratory system, RC705-779
Published
2022
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5. Mining the Plasma Proteome for Insights into the Molecular Pathology of Pulmonary Arterial Hypertension

Author

Lars Harbaum, Christopher J. Rhodes, John Wharton, Allan Lawrie, Jason H. Karnes, Ankit A. Desai, William C. Nichols, Marc Humbert, David Montani, Barbara Girerd, Olivier Sitbon, Mario Boehm, Tatyana Novoyatleva, Ralph T. Schermuly, H. Ardeschir Ghofrani, Mark Toshner, David G. Kiely, Luke S. Howard, Emilia M. Swietlik, Stefan Gräf, Maik Pietzner, Nicholas W. Morrell, Martin R. Wilkins, L Southgate, RD Machado, J Martin, WH Ouwehand, MW Pauciulo, A Arora, K Lutz, F Ahmad, SL Archer, R Argula, ED Austin, D Badesch, S Bakshi, C Barnett, R Benza, N Bhatt, CD Burger, M Chakinala, J Elwing, T Fortin, RP Frantz, A Frost, JGN Garcia, J Harley, H He, NS Hill, R Hirsch, D Ivy, J Klinger, T Lahm, K Marsolo, LJ Martin, SD Nathan, RJ Oudiz, Z Rehman, I Robbins, DM Roden, EB Rosenzweig, G Saydain, R Schilz, RW Simms, M Simon, H Tang, AY Tchourbanov, T Thenappan, F Torres, AK Walsworth, RE Walter, RJ White, J Wilt, D Yung, R Kittles, J Aman, J Knight, KB Hanscombe, H Gall, A Ulrich, HJ Bogaard, C Church, JG Coghlan, R Condliffe, PA Corris, C Danesino, CG Elliott, A Franke, S Ghio, JSR Gibbs, AC Houweling, G Kovacs, M Laudes, RV MacKenzie Ross, S Moledina, M Newnham, A Olschewski, H Olschewski, AJ Peacock, J Pepke-Zaba, L Scelsi, W Seeger, CM Shaffer, O Sitbon, J Suntharalingam, C Treacy, A Vonk Noordegraaf, Q Waisfisz, SJ Wort, RC Trembath, M Germain, I Cebola, J Ferrer, P Amouyel, S Debette, M Eyries, F Soubrier, DA Trégouët, Harbaum, Lars [0000-0002-9422-6195], Lawrie, Allan [0000-0003-4192-9505], Montani, David [0000-0002-9358-6922], Sitbon, Olivier [0000-0002-1942-1951], Gräf, Stefan [0000-0002-1315-8873], Wilkins, Martin R [0000-0003-3926-1171], Apollo - University of Cambridge Repository, British Heart Foundation, and The Academy of Medical Sciences

Subjects
Pulmonary and Respiratory Medicine, Pulmonary Arterial Hypertension, Proteome, case-control studies, Hypertension, Pulmonary, Respiratory System, Blood Proteins, Critical Care and Intensive Care Medicine, Mendelian randomization, Humans, Familial Primary Pulmonary Hypertension, Netrins, Pathology, Molecular, Mendelian randomisation, protein quantitative trait loci, Thrombospondins, genome, 11 Medical and Health Sciences
Abstract

Rationale: Pulmonary arterial hypertension (PAH) is characterized by structural remodeling of pulmonary arteries and arterioles. Underlying biological processes are likely reflected in a perturbation of circulating proteins. Objectives: To quantify and analyze the plasma proteome of patients with PAH using inherited genetic variation to inform on underlying molecular drivers. Methods: An aptamer-based assay was used to measure plasma proteins in 357 patients with idiopathic or heritable PAH, 103 healthy volunteers, and 23 relatives of patients with PAH. In discovery and replication subgroups, the plasma proteomes of PAH and healthy individuals were compared, and the relationship to transplantation-free survival in PAH was determined. To examine causal relationships to PAH, protein quantitative trait loci (pQTL) that influenced protein levels in the patient population were used as instruments for Mendelian randomization (MR) analysis. Measurements and Main Results: From 4,152 annotated plasma proteins, levels of 208 differed between patients with PAH and healthy subjects, and 49 predicted long-term survival. MR based on cis-pQTL located in proximity to the encoding gene for proteins that were prognostic and distinguished PAH from health estimated an adverse effect for higher levels of netrin-4 (odds ratio [OR], 1.55; 95% confidence interval [CI], 1.16-2.08) and a protective effect for higher levels of thrombospondin-2 (OR, 0.83; 95% CI, 0.74-0.94) on PAH. Both proteins tracked the development of PAH in previously healthy relatives and changes in thrombospondin-2 associated with pulmonary arterial pressure at disease onset. Conclusions: Integrated analysis of the plasma proteome and genome implicates two secreted matrix-binding proteins, netrin-4 and thrombospondin-2, in the pathobiology of PAH.

Published
2022

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