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1. Targeting fibroblast phenotype switching in cardiac remodelling as a promising antifibrotic strategy.

Author

Kel, Alexander, Thum, Thomas, and Kunduzova, Oksana

Subjects
GENE regulatory networks, TRANSFORMING growth factors, PHENOTYPIC plasticity, HEART fibrosis, REVERSIBLE phase transitions
Abstract

Myocardial fibrosis, a common feature of heart disease, remains an unsolved clinical challenge. Fibrosis resolution requires activation of cardiac fibroblasts exhibiting context-dependent beneficial and detrimental dichotomy. Here, we explored the hypothesis of fibroblast reversible transition between quiescence and activated myofibroblastic states as a manifestation of cell phenotypic switching in myocardial remodelling. In support, gene regulatory networks executing conversion of cardiac fibroblasts to myofibroblasts and vice versa in fibrosis resolution are reconstructed using TRANSPATH database. In a scenario of fibroblast activation triggered by transforming growth factor β, a cardinal mediator of tissue fibrosis, signalling cascades governing entry into or exit from specific fibroblast statures in cardiac fibrotic remodelling were dissected. It is suggested that fibroblast phenotypic switching constitutes the central gait toward guiding cell state-gating strategies to counteract adverse cardiac fibrosis, a devastating disorder with no approved therapeutic option. [ABSTRACT FROM AUTHOR]

Published
2025
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4. Fibroblast-Specific Protein-Protein Interactions for Myocardial Fibrosis from MetaCore Network.

Author

Frahm, Klaus M., Kotelnikova, Ekaterina, Kunduzova, Oksana, and Shepelyansky, Dima L.

Subjects
MARKOV chain Monte Carlo, PROTEIN-protein interactions, HEART fibrosis, CARDIOVASCULAR diseases, FIBROSIS
Abstract

Myocardial fibrosis is a major pathologic disorder associated with a multitude of cardiovascular diseases (CVD). The pathogenesis is complex and encompasses multiple molecular pathways. Integration of fibrosis-associated genes into the global MetaCore network of protein-protein interactions (PPI) offers opportunities to identify PPI with functional and therapeutic significance. Here, we report the generation of a fibrosis-focused PPI network and identification of fibroblast-specific arbitrators driving reparative and reactive myocardial fibrosis. In TGF- β -mediated fibroblast activation, developed network analysis predicts new regulatory mechanisms for fibrosis-associated genes. We introduce an efficient Erdös barrage approach to suppress activation of a number of fibrosis-associated nodes in order to reverse fibrotic cascades. In the network model each protein node is characterized by an Ising up or down spin corresponding to activated or repairing state acting on other nodes being initially in a neutral state. An asynchronous Monte Carlo process describes fibrosis progression determined by a dominant action of linked proteins. Our results suggest that the constructed Ising Network Fibrosis Interaction model offers network insights into fibrosis mechanisms and can complement future experimental efforts to counteract cardiac fibrosis. [ABSTRACT FROM AUTHOR]

Published
2024
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11. LEOPARD syndrome-associated SHP2 mutation confers leanness and protection from diet-induced obesity

Author

Tajan, Mylène, Batut, Aurélie, Cadoudal, Thomas, Deleruyelle, Simon, Le Gonidec, Sophie, Laurent, Céline Saint, Vomscheid, Maëlle, Wanecq, Estelle, Tréguer, Karine, De Rocca Serra-Nédélec, Audrey, Vinel, Claire, Marques, Marie-Adeline, Pozzo, Joffrey, Kunduzova, Oksana, Salles, Jean-Pierre, Tauber, Maithé, Raynal, Patrick, Cavé, Hélène, Edouard, Thomas, Valet, Philippe, and Yart, Armelle

Published
2014
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12. Age-Related Shift in Cardiac and Metabolic Phenotyping Linked to Inflammatory Cytokines and Antioxidant Status in Mice.

Author

Kang, Ryeonshi, Laborde, Charlotte, Savchenko, Lesia, Swiader, Audrey, Pizzinat, Nathalie, Marsal, Dimitri, Sainte-Marie, Yannis, Boal, Frederic, Tronchere, Helene, Roncalli, Jerome, and Kunduzova, Oksana

Subjects
OXIDANT status, MICE, CYTOKINES, OXIDATIVE stress, RESISTIN, INTERLEUKIN-6, GLUTATHIONE
Abstract

Age-related alterations in cardiac function, metabolic, inflammatory and antioxidant profiles are associated with an increased risk of cardiovascular mortality and morbidity. Here, we examined cardiac and metabolic phenotypes in relation to inflammatory status and antioxidant capacity in young, middle-aged and old mice. Real-time reverse transcription–polymerase chain reactions were performed on myocardium and immunoassays on plasma. Left ventricular (LV) structure and function were assessed by echocardiography using high-frequency ultrasound. Middle-aged mice exhibited an altered metabolic profile and antioxidant capacity compared to young mice, whereas myocardial expression of inflammatory factors (TNFα, IL1β, IL6 and IL10) remained unchanged. In contrast, old mice exhibited increased expression of inflammatory cytokines and plasma levels of resistin compared to young and middle-aged mice (p < 0.05). The pro-inflammatory signature of aged hearts was associated with alterations in glutathione redox homeostasis and elevated contents of 4-hydroxynonenal (4-HNE), a marker of lipid peroxidation and oxidative stress. Furthermore, echocardiographic parameters of LV systolic and diastolic functions were significantly altered in old mice compared to young mice. Taken together, these findings suggest age-related shifts in cardiac phenotype encompass the spectrum of metabo-inflammatory abnormalities and altered redox homeostasis. [ABSTRACT FROM AUTHOR]

Published
2023
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19. Retrospective Study of 573 Patients with Heart Failure Evaluated for Coronary Artery Disease at Toulouse University Center, France

Author

Deney, Antoine, primary, Nader, Vanessa, additional, Matta, Anthony, additional, Itier, Romain, additional, Fournier, Pauline, additional, Lairez, Olivier, additional, Pizzinat, Nathalie, additional, Carrié, Didier, additional, Boal, Frédéric, additional, Galinier, Michel, additional, Kunduzova, Oksana, additional, Azar, Rania, additional, and Roncalli, Jerome, additional

Published
2021
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21. Metformin Attenuates Postinfarction Myocardial Fibrosis and Inflammation in Mice

Author

Loi, Halyna, primary, Kramar, Solomiia, additional, Laborde, Charlotte, additional, Marsal, Dimitri, additional, Pizzinat, Nathalie, additional, Cussac, Daniel, additional, Roncalli, Jerome, additional, Boal, Frederic, additional, Tronchere, Helene, additional, Oleshchuk, Oleksandra, additional, Korda, Mykhaylo, additional, and Kunduzova, Oksana, additional

Published
2021
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22. Towards a Large-Scale Assessment of the Relationship Between Biological and Chronological Aging: The Inspire Mouse Cohort

Author

Santin, Yohan, Lopez, Sébastien, Ader, Isabelle, Andrieu, Sandrine, Blanchard, Nicolas, Carrière, Audrey, Casteilla, Louis, Cousin, Béatrice, Davezac, Noelie, Barreto De Souto, Philipe, Dray, Cédric, Fazilleau, Nicolas, Gonzalez-Dunia, Daniel, Gourdy, Pierre, Guyonnet, Sophie, Jabrane-Ferrat, Nabila, Kunduzova, Oksana, Lezoualc'H, Frank, Liblau, Roland, Martinez, Laurent O., Moro, Cedric, Payoux, Pierre, Pénicaud, Luc, Planat-Benard, Valérie, Rampon, Claire, Rolland, Yves, Schanstra, Joost-Peter, Sierra, Felipe, Valet, Philippe, Varin, Audrey, Vergnolle, Nathalie, Vellas, Bruno, Viña, José, Guiard, Bruno P., Parini, Angelo, Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre de Recherches sur la Cognition Animale (CRCA), Centre National de la Recherche Scientifique (CNRS)-Institut des sciences du cerveau de Toulouse. (ISCT), Université Toulouse - Jean Jaurès (UT2J)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse - Jean Jaurès (UT2J)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre de Biologie Intégrative (CBI), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), STROMALab, Institut National de la Santé et de la Recherche Médicale (INSERM)-Etablissement Français du Sang-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Ecole Nationale Vétérinaire de Toulouse (ENVT), Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS), Epidémiologie et analyses en santé publique : risques, maladies chroniques et handicaps (LEASP), Centre de Physiopathologie Toulouse Purpan ex IFR 30 et IFR 150 (CPTP), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Toulouse Neuro Imaging Center (ToNIC), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Hôpital Purpan [Toulouse], CHU Toulouse [Toulouse]-CHU Toulouse [Toulouse], National Institute on Aging [Bethesda, USA] (NIA), National Institutes of Health [Bethesda] (NIH), Institut de Recherche en Santé Digestive (IRSD ), Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Universitat de València (UV), the Region Occitanie/Pyrenees-Mediterranee (Reference number: 1901175), the European Regional Development Fund (ERDF) (Project number: MP0022856), Inspire Chairs of Excellence - Alzheimer Prevention in Occitania and Catalonia (APOC), EDENIS, KORIAN, Pfizer, Pierre-Fabre, Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, Centre de Biologie Intégrative (CBI), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut des sciences du cerveau de Toulouse. (ISCT), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Toulouse - Jean Jaurès (UT2J)-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Ecole Nationale Vétérinaire de Toulouse (ENVT), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Etablissement Français du Sang-Institut National de la Santé et de la Recherche Médicale (INSERM), Gérontopôle, Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Toulouse [Toulouse], Centre de Physiopathologie Toulouse Purpan (CPTP), Institut de médecine moléculaire de Rangueil (I2MR), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-IFR150-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut National de la Santé et de la Recherche Médicale (INSERM), Universitat Politècnica de València (UPV), Region Occitanie/Pyrenees-Mediterranee (Reference number: 1901175), European Regional Development Fund (ERDF) (Project number: MP0022856), and Inspire Chairs of Excellence funded by: Alzheimer Prevention in Occitania and Catalonia (APOC)

Subjects
Cohort Studies, Male, mouse cohort, Aging, Mice, INSPIRE program, biological aging, [SDV.MHEP.GEG]Life Sciences [q-bio]/Human health and pathology/Geriatry and gerontology, Animals, biomarkers, Female, frailty
Abstract

International audience; Aging is the major risk factor for the development of chronic diseases. After decades of research focused on extending lifespan, current efforts seek primarily to promote healthy aging. Recent advances suggest that biological processes linked to aging are more reliable than chronological age to account for an individual's functional status, i.e. frail or robust. It is becoming increasingly apparent that biological aging may be detectable as a progressive loss of resilience much earlier than the appearance of clinical signs of frailty. In this context, the INSPIRE program was built to identify the mechanisms of accelerated aging and the early biological signs predicting frailty and pathological aging. To address this issue, we designed a cohort of outbred SWISS mice (1576 male and female mice) in which we will continuously monitor spontaneous and voluntary physical activity from 6 to 24 months of age under either normal or high fat/high sucrose diet. At different age points (6, 12, 18, 24 months), multiorgan functional phenotyping will be carried out to identify early signs of organ dysfunction and generate a large biological fluids/feces/organs biobank (100,000 samples). A comprehensive correlation between functional and biological phenotypes will be assessed to determine: 1) the early signs of biological aging and their relationship with chronological age; 2) the role of dietary and exercise interventions on accelerating or decelerating the rate of biological aging; and 3) novel targets for the promotion of healthy aging. All the functional and omics data, as well as the biobank generated in the framework of the INSPIRE cohort will be available to the aging scientific community. The present article describes the scientific background and the strategies employed for the design of the INSPIRE Mouse cohort.

Published
2020
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23. Age-dependent increase in hydrogen peroxide production by cardiac monoamine oxidase A in rats

Author

Maurel, Agnes, Hernandez, Carole, Kunduzova, Oksana, Bompart, Guy, Cambon, Claudie, Parini, Angelo, and Frances, Bernard

Subjects
Physiology -- Research, Oxidation-reduction reaction -- Physiological aspects, Monoamine oxidase -- Physiological aspects, Hydrogen peroxide -- Physiological aspects, Biological sciences
Abstract

Oxidative stress is one of the factors involved in age-related impairment of cardiac function. In the present study, we investigated the role of the catecholamine-degrading enzyme monoamine oxidase (MAO) in [H.sub.2][O.sub.2] production in the hearts of young, adult, and old rats. MAO-dependent [H.sub.2[O.sub.2] production, measured by a chemiluminescence-based assay, increased with age, reaching the maximum in 24-mo-old rats (7.5-fold increase vs. 1-mo-old rats). The following observations indicate that the age-dependent increase in [H.sub.2][O.sub.2] generation was fully related to the MAO-A isoform: 1) at all the ages tested, chemiluminescence production was inhibited by the MAO-A inhibitor clorgyline but not by the MAO-B inhibitor RO-19 6327; 2) enzyme assay, Western blot, and semiquantitative RT-PCR analysis showed an age-dependent increase in cardiac MAO-A activity, immunodetection, and mRNA expression, respectively; and 3) the MAO-B isoform was undetectable by enzyme assay and Western blot analysis. These results suggest that MAO-A could be a major source of [H.sub.2][O.sub.2] in the aging heart. monoamine oxidases; oxidative stress

Published
2003

25. Apilimod alters TGFβ signaling pathway and prevents cardiac fibrotic remodeling

Author

Cinato, Mathieu, primary, Guitou, Laurie, additional, Saidi, Amira, additional, Timotin, Andrei, additional, Sperazza, Erwan, additional, Duparc, Thibaut, additional, Zolov, Sergey N., additional, Giridharan, Sai Srinivas Panapakkam, additional, Weisman, Lois S., additional, Martinez, Laurent O., additional, Roncalli, Jerome, additional, Kunduzova, Oksana, additional, Tronchere, Helene, additional, and Boal, Frederic, additional

Published
2021
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26. Détermination de Propriété Diélectrique d’un Système Biologique

Author

Wang, J.-Y, Benmohamed, Faycal, Tao, Junwu, Kunduzova, Oksana, Tao, Junwu, Groupe de Recherche en Electromagnétisme (LAPLACE-GRE), LAboratoire PLasma et Conversion d'Energie (LAPLACE), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Centre National de la Recherche Scientifique (CNRS)-Institut National Polytechnique (Toulouse) (Toulouse INP), Université Fédérale Toulouse Midi-Pyrénées-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées, Laboratoire Hubert Curien [Saint Etienne] (LHC), Institut d'Optique Graduate School (IOGS)-Université Jean Monnet [Saint-Étienne] (UJM)-Centre National de la Recherche Scientifique (CNRS), Institut National Polytechnique (Toulouse) (Toulouse INP), Institut des Maladies Métaboliques et Casdiovasculaires (UPS/Inserm U1297 - I2MC), and Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)

Subjects
[SDV] Life Sciences [q-bio], [SPI.ELEC]Engineering Sciences [physics]/Electromagnetism, [SDV]Life Sciences [q-bio], [SPI.ELEC] Engineering Sciences [physics]/Electromagnetism, [SPI.MAT]Engineering Sciences [physics]/Materials
Abstract

International audience;  L'extraction de propriété diélectrique équivalente des solutions aqueuses utilisées dans l'exposition des systèmes biologiques aux champs électromagnétiques radiofréquence a été réalisée à l'aide d'une cellule de mesure en ligne planaire et plusieurs méthodes d'analyse électromagnétique de l'ensemble de structure. La méthode d'extraction a été validée sur des échantillons des produits de références connues. Des études ont été menées sur un liquide utilisé pour la culture des cellules cardiaques pour son exposition aux champs électromagnétiques, permettant l'évaluation du Débit d'Absorption Spécifique (DAS), et par la suite le dimensionnement du système d'exposition, notamment en terme de la puissance appliquée. I.

Published
2020

29. Metformin Protects the Heart Against Hypertrophic and Apoptotic Remodeling After Myocardial Infarction

Author

Loi, Halyna, Boal, Frederic, Tronchere, Helene, Cinato, Mathieu, Kramar, Solomiia, Oleshchuk, Oleksandra, Korda, Mykhaylo, and Kunduzova, Oksana

Subjects
Pharmacology, myocardial infarction, endocrine system diseases, cardiovascular system, apoptosis, nutritional and metabolic diseases, Pharmacology (medical), cardiac remodeling, metformin, hypertrophy, Original Research
Abstract

Cardiovascular complications are the most prevalent cause of morbidity and mortality in diabetic patients. Metformin is currently the first-line blood glucose-lowering agent with potential relevance to cardiovascular diseases. However, the underpinning mechanisms of action remain elusive. Here, we report that metformin represses cardiac apoptosis at least in part through inhibition of Forkhead box O1 (FoxO1) pathway. In a mouse model of ischemia-reperfusion (I/R), treatment with metformin attenuated cardiac and hypertrophic remodeling after 14 days of post-reperfusion. Additionally, cardiac expression of brain-like natriuretic peptide (BNP) was significantly reduced in metformin-treated mice after 14 days of cardiac I/R. In cultured H9C2 cells, metformin counteracted hypertrophic and apoptotic responses to metabolic or hypoxic stress. FoxO1 silencing by siRNA abolished anti-apoptotic effect of metformin under hypoxic stress in H9C2 cells. Taken together, these results suggest that metformin protects the heart against hypertrophic and apoptotic remodeling after myocardial infarction.

Published
2019

34. Cardioprotective properties of N-terminal galanin fragment (2-15) in experimental ischemia/reperfusion injury

Author

Pisarenko, Oleg, primary, Timotin, Andrei, additional, Sidorova, Maria, additional, Studneva, Irina, additional, Shulzhenko, Valentin, additional, Palkeeva, Marina, additional, Serebryakova, Larisa, additional, Molokoedov, Aleksander, additional, Veselova, Oksana, additional, Cinato, Mathieu, additional, Boal, Frederic, additional, Tronchere, Helene, additional, and Kunduzova, Oksana, additional

Published
2017
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35. Myocardial protection from ischemia/reperfusion injury by exogenous galanin fragment

Author

Timotin, Andrei, primary, Pisarenko, Oleg, additional, Sidorova, Maria, additional, Studneva, Irina, additional, Shulzhenko, Valentin, additional, Palkeeva, Marina, additional, Serebryakova, Larisa, additional, Molokoedov, Aleksander, additional, Veselova, Oksana, additional, Cinato, Mathieu, additional, Tronchere, Helene, additional, Boal, Frederic, additional, and Kunduzova, Oksana, additional

Published
2017
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36. Apelin regulates FoxO3 translocation to mediate cardioprotective responses to myocardial injury and obesity

Author

Boal, Frederic, primary, Roumegoux, Jessica, additional, Alfarano, Chiara, additional, Timotin, Andrei, additional, Calise, Denis, additional, Anesia, Rodica, additional, Drougard, Anne, additional, Knauf, Claude, additional, Lagente, Christine, additional, Roncalli, Jerome, additional, Desmoulin, Franck, additional, Tronchere, Helene, additional, Valet, Philippe, additional, Parini, Angelo, additional, and Kunduzova, Oksana, additional

Published
2015
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38. Apelin prevents cardiac fibroblast activation and collagen production through inhibition of sphingosine kinase 1

Author

Pchejetski, Dmitri, primary, Foussal, Camille, additional, Alfarano, Chiara, additional, Lairez, Olivier, additional, Calise, Denis, additional, Guilbeau-Frugier, Celine, additional, Schaak, Stéphane, additional, Seguelas, Marie-Hélène, additional, Wanecq, Estelle, additional, Valet, Philippe, additional, Parini, Angelo, additional, and Kunduzova, Oksana, additional

Published
2011
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42. PI5P Triggers ICAM-1 Degradation in ShigellaInfected Cells, Thus Dampening Immune Cell Recruitment

Author

Boal, Frédéric, Puhar, Andrea, Xuereb, Jean-Marie, Kunduzova, Oksana, Sansonetti, Philippe J., Payrastre, Bernard, and Tronchère, Hélène

Abstract

Shigella flexneri, the pathogen responsible for bacillary dysentery, has evolved multiple strategies to control the inflammatory response. Here, we show that Shigellasubverts the subcellular trafficking of the intercellular adhesion molecule-1 (ICAM-1), a key molecule in immune cell recruitment, in a mechanism dependent on the injected bacterial enzyme IpgD and its product, the lipid mediator PI5P. Overexpression of IpgD, but not a phosphatase dead mutant, induced the internalization and the degradation of ICAM-1 in intestinal epithelial cells. Remarkably, addition of permeant PI5P reproduced IpgD effects and led to the inhibition of neutrophil recruitment. Finally, these results were confirmed in an in vivo model of Shigellainfection where IpgD-dependent ICAM-1 internalization reduced neutrophil adhesion. In conclusion, we describe here an immune evasion mechanism used by the pathogen Shigellato divert the host cell trafficking machinery in order to reduce immune cell recruitment.

Published
2016
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43. Fibrosis Protein-Protein Interactions from Google Matrix Analysis of MetaCore Network.

Author

Kotelnikova, Ekaterina, Frahm, Klaus M., Shepelyansky, Dima L., and Kunduzova, Oksana

Subjects
PROTEIN-protein interactions, FIBROSIS, HEART fibrosis, HEART failure, DRUG target
Abstract

Protein–protein interactions is a longstanding challenge in cardiac remodeling processes and heart failure. Here, we use the MetaCore network and the Google matrix algorithms for prediction of protein–protein interactions dictating cardiac fibrosis, a primary cause of end-stage heart failure. The developed algorithms allow identification of interactions between key proteins and predict new actors orchestrating fibroblast activation linked to fibrosis in mouse and human tissues. These data hold great promise for uncovering new therapeutic targets to limit myocardial fibrosis. [ABSTRACT FROM AUTHOR]

Published
2022
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44. Myocardial capacity of mitochondrial oxidative phosphorylation in response to prolonged electromagnetic stress.

Author

Savchenko L, Martinelli I, Marsal D, Zhdan V, Tao J, and Kunduzova O

Abstract

Introduction: Mitochondria are central energy generators for the heart, producing adenosine triphosphate (ATP) through the oxidative phosphorylation (OXPHOS) system. However, mitochondria also guide critical cell decisions and responses to the environmental stressors., Methods: This study evaluated whether prolonged electromagnetic stress affects the mitochondrial OXPHOS system and structural modifications of the myocardium. To induce prolonged electromagnetic stress, mice were exposed to 915 MHz electromagnetic fields (EMFs) for 28 days., Results: Analysis of mitochondrial OXPHOS capacity in EMF-exposed mice pointed to a significant increase in cardiac protein expression of the Complex I, II, III and IV subunits, while expression level of α-subunit of ATP synthase (Complex V) was stable among groups. Furthermore, measurement of respiratory function in isolated cardiac mitochondria using the Seahorse XF24 analyzer demonstrated that prolonged electromagnetic stress modifies the mitochondrial respiratory capacity. However, the plasma level of malondialdehyde, an indicator of oxidative stress, and myocardial expression of mitochondria-resident antioxidant enzyme superoxide dismutase 2 remained unchanged in EMF-exposed mice as compared to controls. At the structural and functional state of left ventricles, no abnormalities were identified in the heart of mice subjected to electromagnetic stress., Discussion: Taken together, these data suggest that prolonged exposure to EMFs could affect mitochondrial oxidative metabolism through modulating cardiac OXPHOS system., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (© 2023 Savchenko, Martinelli, Marsal, Zhdan, Tao and Kunduzova.)

Published
2023
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