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20. Catalyzing transcriptomics research in cardiovascular disease: The CardioRNA COST action CA17129

Author

Da Costa Gomes, Clarissa Pedrosa, Ágg, Bence, Andova, Andrejaana, Arslan, Serdal, Baker, Andrew, Barteková, Monika, Beis, Dimitris, Betsou, Fay, Bezzina Wettinger, Stephanie, Bugarski, Branko, Condorelli, Gianluigi, Da Silva, Gustavo José Justo, Danilin, Sabrina, De Gonzalo-Calvo, David, Buil, Alfonso, Carmo-Fonseca, Maria, Enguita, Francisco J., Felekkis, Kyriacos, Ferdinandy, Peter, Gyöngyösi, Mariann, Hackl, Matthias, Karaduzovic-Hadziabdic, Kanita, Hellemans, Jan, Heymans, Stephane, Hlavackova, Markéta, Hoydal, Morten Andre, Jankovic, Aleksandra, Jusic, Amela, Kardassis, Dimitris, Kerkelä, Risto, Kuster, Gabriela M., Lakkisto, Päivi, Leszek, Przemyslaw, Lustrek, Mitja, Maegdefessel, Lars, Martelli, Fabio, Novella, Susana, O’Brien, Timothy, Papaneophytou, Christos, Pedrazzini, Thierry, Pinet, Florence, Popescu, Octavian, Potoˇcnjak, Ines, Robinson, Emma L., Sasson, Shlomo, Scholz, Markus, Simionescu, Maya, Stoll, Monika, Varga, Zoltan V., Vinciguerra, Manlio, Xuereb, Angela, Yilmaz, Mehmet Birhan, Emanueli, Costanza, Devaux, Yvan, Formosa, Melissa Marie, EU-CardioRNA COST Action (CA17129), Repositório da Universidade de Lisboa, Luxembourg Institute of Health (LIH), Semmelweis University [Budapest], Jozef Stefan Institute [Ljubljana] (IJS), Cumhuriyet University [Sivas, Turkey], Queen's Medical Researche Institute, University of Edinburgh, Slovak Academy of Sciences (SAS), Biomedical Research Foundation of the Academy of Athens (BRFAA), Integrated BioBank of Luxembourg (IBBL), University of Malta [Malta], Faculty of Technology and Metallurgy [University of Belgrade], University of Belgrade [Belgrade], Humanitas Clinical and Research Center [Rozzano, Milan, Italy], Oslo University Hospital [Oslo], University of Oslo (UiO), Firalis SAS, Spanish National Research Council (CSIC), Universidade de Lisboa (ULISBOA), University of Cyprus [Nicosia], Medizinische Universität Wien = Medical University of Vienna, International University of Sarajevo, Maastricht University [Maastricht], Czech Academy of Sciences [Prague] (CAS), Norwegian University of Science and Technology [Trondheim] (NTNU), Norwegian University of Science and Technology (NTNU), Institute for Biological Research Sinisa Stankovic [Belgrade] (IBISS), University of Tuzla, University of Crete [Heraklion] (UOC), Institute of Molecular Biology and Biotechnology (IMBB-FORTH), Foundation for Research and Technology - Hellas (FORTH), University of Oulu, University Hospital Basel [Basel], University of Basel (Unibas), Minerva Foundation Institute for Medical Research, Karolinska Institutet [Stockholm], Istituti di Ricovero e Cura a Carattere Scientifico (IRCCS), Universitat de València (UV), National University of Ireland [Galway] (NUI Galway), Université de Lausanne (UNIL), Facteurs de Risque et Déterminants Moléculaires des Maladies liées au Vieillissement - U 1167 (RID-AGE), 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), Babes-Bolyai University [Cluj-Napoca] (UBB), The Hebrew University of Jerusalem (HUJ), Leipzig University, Institute of Cellular Biology and Pathology Nicolae Simionescu, Westfälische Wilhelms-Universität Münster (WWU), Dokuz Eylül Üniversitesi = Dokuz Eylül University [Izmir] (DEÜ), National Heart and Lung Institute [London] (NHLI), Royal Brompton and Harefield NHS Foundation Trust-Imperial College London, EU-CardioRNA COST Action (CA17129), European Cooperation in Science and Technology, [Gomes, Clarissa Pedrosa da Costa -- Devaux, Yvan] Luxembourg Inst Hlth, Cardiovasc Res Unit, L-1445 Strassen, Luxembourg -- [Agg, Bence -- Ferdinandy, Peter -- Varga, Zoltan V.] Semmelweis Univ, Dept Pharmacol & Pharmacotherapy, H-1085 Budapest, Hungary -- [Andova, Andrejaana -- Lustrek, Mitja] Jozef Stefan Inst, Dept Intelligent Syst, Ljubljana 1000E, Slovenia -- [Arslan, Serdal] Cumhuriyet Univ, Fac Med, Dept Med Biol, TR-58140 Sivas, Turkey -- [Baker, Andrew] Univ Edinburgh, Ctr Cardiovasc Sci, Queens Med Res Inst, Edinburgh EH16 4TJ, Midlothian, Scotland -- [Bartekova, Monika] Slovak Acad Sci, Ctr Expt Med, Inst Heart Res, Bratislava 84104, Slovakia -- [Beis, Dimitris] Acad Athens, Biomed Res Fdn, Athens 11527, Greece -- [Betsou, Fay] Integrated BioBank Luxembourg, L-3550 Dudelange, Luxembourg -- [Wettinger, Stephanie Bezzina -- Xuereb, Angela] Univ Malta, Fac Hlth Sci, MSD-2080 Msida, Malta -- [Bugarski, Branko] Univ Belgrade, Fac Technol & Met, Belgrade 11000, Serbia -- [Condorelli, Gianluigi] Humanitas Res Hosp, Dept Cardiovasc, I-20089 Rozzano, Italy -- [da Silva, Gustavo Jose Justo] Oslo Univ Hosp, Inst Expt Med Res, PB 4956 Nydalen, NO-0424 Oslo, Norway -- [da Silva, Gustavo Jose Justo] Univ Oslo, PB 4956 Nydalen, NO-0424 Oslo, Norway -- [Danilin, Sabrina] Firalis, F-68330 Huningue, France -- [de Gonzalo-Calvo, David] CSIC, Inst Biomed Res Barcelona IIBB, Barcelona 08036, Spain -- [Buil, Alfonso] Mental Hlth Ctr Sct Hans, DK-4000 Roskilde, Denmark -- [Carmo-Fonseca, Maria -- Enguita, Francisco J.] Univ Lisbon, Fac Med, Inst Med Mol, P-1649028 Lisbon, Portugal -- [Felekkis, Kyriacos -- Papaneophytou, Christos] Univ Nicosia, Sch Sci & Engn, Dept Life & Hlth Sci, CY-2417 Nicosia, Cyprus -- [Gyoengyoesi, Mariann] Med Univ Vienna, Dept Cardiol, A-1090 Vienna, Austria -- [Hackl, Matthias] TAmiRNA, A-1190 Vienna, Austria -- [Karaduzovic-Hadziabdic, Kanita] Int Univ Sarajevo, Fac Engn & Nat Sci, Sarajevo 71210, Bosnia & Herceg -- [Hellemans, Jan] Biogazelle, B-9052 Zwijnaarde, Belgium -- [Heymans, Stephane] Maastricht Univ, Fac Hlth Med & Life Sci, Sch Cardiovasc Dis, NL-6229 ER Maastricht, Netherlands -- [Hlavackova, Marketa] Czech Acad Sci, Inst Physiol, Dept Dev Cardiol, Prague 14220, Czech Republic -- [Hoydal, Morten Andre] NTNU Norwegian Univ Technol & Sci, Fac Med & Hlth Sci, Dept Circulat & Med Imaging, NO-7489 Trondheim, Norway -- [Jankovic, Aleksandra] Univ Belgrade, Inst Biol Res Sinisa Stankovic, Dept Physiol, Belgrade 11000, Serbia -- [Jusic, Amela] Univ Tuzla, Fac Nat Sci & Math, Dept Biol, Tuzla 75000, Bosnia & Herceg -- [Kardassis, Dimitris] Univ Crete, Med Sch, Dept Basic Sci, Iraklion 71003, Crete, Greece -- [Kardassis, Dimitris] Fdn Res & Technol Hellas, Inst Mol Biol & Biotechnol, Iraklion 71003, Crete, Greece -- [Kerkela, Risto] Univ Oulu, Res Unit Biomed, Oulu 90014, Finland -- [Kuster, Gabriela M.] Univ Hosp, Dept Biomed & Clin Cardiol, CH-4031 Basel, Switzerland -- [Kuster, Gabriela M.] Univ Basel, CH-4031 Basel, Switzerland -- [Lakkisto, Paivi] Minerva Fdn, Helsinki 00290, Finland -- [Leszek, Przemyslaw] Cardinal Stefan Wyszynski Inst Cardiol, PL-04628 Warsaw, Poland -- [Maegdefessel, Lars] Karolinska Inst, Ctr Mol Med, S-17176 Stockholm, Sweden -- [Martelli, Fabio] IRCCS Policlin San Donato, Mol Cardiol Lab, I-20097 Milan, Italy -- [Novella, Susana] Univ Valencia, Dept Physiol, Valencia 46010, Spain -- [Novella, Susana] INCLIVA Biomed Res Inst INCLIVA, Valencia 46010, Spain -- [O'Brien, Timothy] Natl Univ Ireland Galway, Regenerat Med Inst REMEDI, Galway H91 TK33, Ireland -- [Pedrazzini, Thierry] Univ Lausanne, Med Sch, Dept Cardiovasc Med, Expt Cardiol Unit,Div Cardiol, CH-1011 Lausanne, Switzerland -- [Pinet, Florence] Inst Pasteur, INSERM, F-59019 Lille, France -- [Popescu, Octavian] Babes Bolyai Univ, Cluj Napoca 400084, Romania -- [Potocnjak, Ines] Univ Hosp Ctr Sisters Char, Inst Clin Med Res & Educ, Zagreb 10000, Croatia -- [Robinson, Emma] Maastricht Univ, Fac Hlth Med & Life Sci, Ctr Heart Failure Res, Dept Cardiol, NL-6229 ER Maastricht, Netherlands -- [Sasson, Shlomo] Hebrew Univ Jerusalem, Fac Med, Inst Drug Res, IL-91120 Jerusalem, Israel -- [Scholz, Markus] Univ Leipzig, Med Fac, Inst Med Informat Stat & Epidemiol, D-04107 Leipzig, Germany -- [Simionescu, Maya] Inst Cellular Biol & Pathol Nicolae Simionescu, Bucharest 050568, Romania -- [Stoll, Monika] Westfalische Wilhelms Univ Munster, Inst Human Genet, Dept Genet Epidemiol, D-48149 Munster, Germany -- [Vinciguerra, Manlio] Int Clin Res Ctr, Brno 65691, Czech Republic -- [Yilmaz, Mehmet Birhan] Dokuz Eylul Univ, Fac Med, Dept Cardiol, TR-35340 Izmir, Turkey -- [Emanueli, Costanza] Imperial Coll London, Fac Med, Natl Heart & Lung Inst, London W12 0HH, England, Hlavackova, Marketa -- 0000-0003-3842-6907, Devaux, Yvan -- 0000-0002-5321-8543, Gyongyosi, Mariann -- 0000-0002-7083-2107, Sasson, Shlomo -- 0000-0002-9343-526X, Buil, Alfonso -- 0000-0002-3097-1014, Hoydal, Morten -- 0000-0003-1804-2578, Justo da Silva, Gustavo -- 0000-0002-1651-7966, Baker, Andrew -- 0000-0003-1441-5576, Lakkisto, Paivi -- 0000-0001-9935-6573, Pinet, Florence -- 0000-0002-5471-1487, Martelli, Fabio -- 0000-0002-8624-7738, Robinson, Emma -- 0000-0002-4866-731X, Novella, Susana -- 0000-0001-8303-7252, Jusic, Amela -- 0000-0003-2835-4284, Beis, Dimitris -- 0000-0003-2579-7848, O'Brien, Timothy -- 0000-0001-9028-5481, Popescu, Octavian -- 0000-0002-2597-7155, Felekkis, Kyriacos -- 0000-0002-0919-0037, de Gonzalo Calvo, David -- 0000-0003-2240-3532, Universidade de Lisboa = University of Lisbon (ULISBOA), University of Cyprus [Nicosia] (UCY), Université de Lausanne = University of Lausanne (UNIL), Westfälische Wilhelms-Universität Münster = University of Münster (WWU), Imperial College London-Royal Brompton and Harefield NHS Foundation Trust, Cardiologie, MUMC+: MA Med Staf Spec Cardiologie (9), RS: CARIM - R2.02 - Cardiomyopathy, RS: CARIM - R2 - Cardiac function and failure, and RS: Carim - H02 Cardiomyopathy

Subjects
Project Report, 0301 basic medicine, medicine.medical_specialty, Biochemistry & Molecular Biology, Knowledge management, lcsh:QH426-470, BIOMARKERS, best practices and guidelines, cardiovascular disease, personalized medicine, transcriptomics, translational research, Context (language use), Translational research, Disease, 030204 cardiovascular system & hematology, Biology, Biochemistry, LONG NONCODING RNAS, 03 medical and health sciences, 0302 clinical medicine, [SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system, CIRCULATING MICRORNAS, TARGETS, Genetics, medicine, Cost action, Set (psychology), Molecular Biology, ComputingMilieux_MISCELLANEOUS, Genetics & Heredity, Science & Technology, business.industry, Cardiovascular system -- Diseases, Public health, Medicine -- Research -- International cooperation, 3. Good health, lcsh:Genetics, 030104 developmental biology, Action (philosophy), PERSPECTIVES, Personalized medicine, Translational research, biomedical, business, Transcriptome, Life Sciences & Biomedicine
Abstract

WOS: 000474931400001, PubMed ID: 30934986, Cardiovascular disease (CVD) remains the leading cause of death worldwide and, despite continuous advances, better diagnostic and prognostic tools, as well as therapy, are needed. The human transcriptome, which is the set of all RNA produced in a cell, is much more complex than previously thought and the lack of dialogue between researchers and industrials and consensus on guidelines to generate data make it harder to compare and reproduce results. This European Cooperation in Science and Technology (COST) Action aims to accelerate the understanding of transcriptomics in CVD and further the translation of experimental data into usable applications to improve personalized medicine in this field by creating an interdisciplinary network. It aims to provide opportunities for collaboration between stakeholders from complementary backgrounds, allowing the functions of different RNAs and their interactions to be more rapidly deciphered in the cardiovascular context for translation into the clinic, thus fostering personalized medicine and meeting a current public health challenge. Thus, this Action will advance studies on cardiovascular transcriptomics, generate innovative projects, and consolidate the leadership of European research groups in the field. COST (European Cooperation in Science and Technology) is a funding organization for research and innovation networks (www.cost.eu)., COST (European Cooperation in Science and Technology) Action EU-CardioRNA [CA17129], This work is supported by COST (European Cooperation in Science and Technology) Action EU-CardioRNA CA17129. YD is the chair and CE is the vice-chair of the European COST Action CA17129, CardioRNA.

Published
2019

25. Signaling and cytotoxic functions of 4-hydroxyalkenals

Author

Riahi, Yael, Cohen, Guy, Shamni, Ofer, and Sasson, Shlomo

Subjects
Oxidation-reduction reaction -- Research, Metabolites -- Physiological aspects, Metabolites -- Chemical properties, Unsaturated fatty acids -- Physiological aspects, Unsaturated fatty acids -- Chemical properties, Biological sciences
Abstract

The peroxidation of n-3 and n-6 polyunsaturated fatty acids (PUFAs) and of their hydroperoxy metabolites is a complex process. It is initiated by free oxygen radical-induced abstraction of a hydrogen atom from the lipid molecule followed by a series of nonenzymatic reactions that ultimately generate the reactive aldehyde species 4-hydroxyalkenals. The molecule 4-hydroxy-2E-hexenal (4-HHE) is generated by peroxidation of n-3 PUFAs, such as linolenic acid, eicosapentaenoic acid, and docosahexaenoic acid. The aldehyde product 4-hydroxy-2E-nonenal (4-HNE) is the peroxidation product of n-6 PUFAs, such as arachidonic and linoleic acids and their 15-lipoxygenase metabolites, namely 15-hydroperoxyeicosatetraenoic acid (15-HpETE) and 13-hydroperoxyoctadecadienoic acid (13-HpODE). Another reactive peroxidation product is 4-hydroxy-2E,6Z-dodecadienal (4-HDDE), which is derived from 12-hydroperoxyeicosatetraenoic acid (12-HpETE), the 12-lipoxygenase metabolite of arachidonic acid. Hydroxyalkenals, notably 4-HNE, have been implicated in various pathophysiological interactions due to their chemical reactivity and the formation of covalent adducts with macromolecules. The progressive accumulation of these adducts alters normal cell functions that can lead to cell death. The lipophilicity of these aldehydes positively correlates to their chemical reactivity. Nonetheless, at low and noncytotoxic concentrations, these molecules may function as signaling molecules in cells. This has been shown mostly for 4-HNE and to some extent for 4-HHE. The capacity of 4-HDDE to generate such 'mixed signals' in cells has received less attention. This review addresses the origin and cellular functions of 4-hydroxyalkernals. lipid peroxidation; diabetes; reactive oxygen species; 4-hydroxyhexenal; 4-hydroxynonenal; 4-hydroxydodecadienal; lipoxygenase; polyunsaturated fatty acids doi: 10.1152/ajpendo.00508.2010.

Published
2010

26. Investigation of the Membrane Fluidity Regulation of Fatty Acid Intracellular Distribution by Fluorescence Lifetime Imaging of Novel Polarity Sensitive Fluorescent Derivatives

Author

Bianchetti, Giada, primary, Azoulay-Ginsburg, Salome, additional, Keshet-Levy, Nimrod Yosef, additional, Malka, Aviv, additional, Zilber, Sofia, additional, Korshin, Edward E., additional, Sasson, Shlomo, additional, De Spirito, Marco, additional, Gruzman, Arie, additional, and Maulucci, Giuseppe, additional

Published
2021
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34. Function of estrogen receptor tyrosine 537 in hormone binding, DNA binding, and transactivation

Author

Yudt, Matthew R., Vorojeikina, Daria, Zhong, Li, Skafar, Debra F., Sasson, Shlomo, Notides, Angelo C., and Gasiewicz, Thomas A.

Subjects
Biochemistry -- Research, Carrier proteins -- Physiological aspects, Cellular signal transduction -- Physiological aspects, Biological sciences, Chemistry
Abstract

Study of human estrogen receptor (hER) Y537 has been continued to resolve some apparent contradictions. A model in which Y537 mutation favors an open pocket conformation is proposed. It affects the estrogen binding kinetics and stability of the hormone-bound, transcriptionally active closed pocket arrangement. The Y537F mutation does not significantly change the hER affinity for the estrogen response element or estrogenic ligands.

Published
1999

38. Catalyzing Transcriptomics Research in Cardiovascular Disease: The CardioRNA COST Action CA17129

Author

Gomes, Clarissa Pedrosa da C, Ágg, Bence, Andova, Andrejaana, Arslan, Serdal, Baker, Andrew, Barteková, Monika, Beis, Dimitris, Betsou, Fay, Wettinger, Stephanie Bezzina, Bugarski, Branko, Condorelli, Gianluigi, da Silva, Gustavo Jose Justo, Danilin, Sabrina, de Gonzalo-Calvo, David, Buil, Alfonso, Carmo-Fonseca, Maria, Enguita, Francisco J, Felekkis, Kyriacos, Ferdinandy, Peter, Gyöngyösi, Mariann, Hackl, Matthias, Karaduzović-Hadžiabdić, Kanita, Hellemans, Jan, Heymans, Stephane, Hlavackova, Markéta, Hoydal, Morten Andre, Janković, Aleksandra, Jusić, Amela, Kardassis, Dimitris, Kerkelä, Risto, Kuster, Gabriela M, Lakkisto, Päivi, Leszek, Przemyslaw, Lustrek, Mitja, Maegdefessel, Lars, Martelli, Fabio, Novella, Susana, O'Brien, Timothy, Papaneophytou, Christos, Pedrazzini, Thierry, Pinet, Florence, Popescu, Octavian, Potočnjak, Ines, Robinson, Emma, Sasson, Shlomo, Scholz, Markus, Simionescu, Maya, Stoll, Monika, Varga, Zoltan V, Vinciguerra, Manlio, Xuereb, Angela, Yilmaz, Mehmet Birhan, Emanueli, Costanza, Devaux, Yvan, Gomes, Clarissa Pedrosa da C, Ágg, Bence, Andova, Andrejaana, Arslan, Serdal, Baker, Andrew, Barteková, Monika, Beis, Dimitris, Betsou, Fay, Wettinger, Stephanie Bezzina, Bugarski, Branko, Condorelli, Gianluigi, da Silva, Gustavo Jose Justo, Danilin, Sabrina, de Gonzalo-Calvo, David, Buil, Alfonso, Carmo-Fonseca, Maria, Enguita, Francisco J, Felekkis, Kyriacos, Ferdinandy, Peter, Gyöngyösi, Mariann, Hackl, Matthias, Karaduzović-Hadžiabdić, Kanita, Hellemans, Jan, Heymans, Stephane, Hlavackova, Markéta, Hoydal, Morten Andre, Janković, Aleksandra, Jusić, Amela, Kardassis, Dimitris, Kerkelä, Risto, Kuster, Gabriela M, Lakkisto, Päivi, Leszek, Przemyslaw, Lustrek, Mitja, Maegdefessel, Lars, Martelli, Fabio, Novella, Susana, O'Brien, Timothy, Papaneophytou, Christos, Pedrazzini, Thierry, Pinet, Florence, Popescu, Octavian, Potočnjak, Ines, Robinson, Emma, Sasson, Shlomo, Scholz, Markus, Simionescu, Maya, Stoll, Monika, Varga, Zoltan V, Vinciguerra, Manlio, Xuereb, Angela, Yilmaz, Mehmet Birhan, Emanueli, Costanza, and Devaux, Yvan

Abstract

Cardiovascular disease (CVD) remains the leading cause of death worldwide and, despite continuous advances, better diagnostic and prognostic tools, as well as therapy, are needed. The human transcriptome, which is the set of all RNA produced in a cell, is much more complex than previously thought and the lack of dialogue between researchers and industrials and consensus on guidelines to generate data make it harder to compare and reproduce results. This European Cooperation in Science and Technology (COST) Action aims to accelerate the understanding of transcriptomics in CVD and further the translation of experimental data into usable applications to improve personalized medicine in this field by creating an interdisciplinary network. It aims to provide opportunities for collaboration between stakeholders from complementary backgrounds, allowing the functions of different RNAs and their interactions to be more rapidly deciphered in the cardiovascular context for translation into the clinic, thus fostering personalized medicine and meeting a current public health challenge. Thus, this Action will advance studies on cardiovascular transcriptomics, generate innovative projects, and consolidate the leadership of European research groups in the field. COST (European Cooperation in Science and Technology) is a funding organization for research and innovation networks (www.cost.eu).

Published
2019

39. Catalyzing transcriptomics research in cardiovascular disease: the CardioRNA COST action CA17129

Author

European Cooperation in Science and Technology, Pedrosa da Costa Gomes, Clarissa, Ágg, Bence, Andova, Andrejaana, Arslan, Serdal, Baker, Andrew, Barteková, Monika, Beis, Dimitris, Betsou, Fay, Bezzina Wettinger, Stephanie, Bugarski, Branko, Condorelli, Gianluigi, Silva, Gustavo José Justo da, Danilin, Sabrina, Gonzalo-Calvo, David de, Buil, Alfonso, Carmo-Fonseca, Maria, Enguita, Francisco J., Felekkis, Kyriacos, Ferdinandy, Peter, Gyöngyösi, Mariann, Hackl, Matthias, Karaduzovic-Hadziabdic, Kanita, Hellemans, Jan, Heymans, Stephane, Hlavackova, Markéta, Hoydal, Morten Andre, Jankovic, Aleksandra, Jusic, Amela, Kardassis, Dimitris, Kerkelä, Risto, Kuster, Gabriela M., Lakkisto, Päivi, Leszek, Przemyslaw, Lustrek, Mitja, Maegdefessel, Lars, Martelli, Fabio, Novella, Susana, O’Brien, Timothy, Papaneophytou, Christos, Pedrazzini, Thierry, Pinet, Florence, Popescu, Octavian, Potočnjak, Ines, Robinson, Emma, Sasson, Shlomo, Scholz, Markus, Simionescu, Maya, Stoll, Monika, Varga, Zoltan V., Vinciguerra, Manlio, Xuereb, Angela, Yilmaz, Mehmet Birhan, Emanueli, Costanza, Devaux, Yvan, European Cooperation in Science and Technology, Pedrosa da Costa Gomes, Clarissa, Ágg, Bence, Andova, Andrejaana, Arslan, Serdal, Baker, Andrew, Barteková, Monika, Beis, Dimitris, Betsou, Fay, Bezzina Wettinger, Stephanie, Bugarski, Branko, Condorelli, Gianluigi, Silva, Gustavo José Justo da, Danilin, Sabrina, Gonzalo-Calvo, David de, Buil, Alfonso, Carmo-Fonseca, Maria, Enguita, Francisco J., Felekkis, Kyriacos, Ferdinandy, Peter, Gyöngyösi, Mariann, Hackl, Matthias, Karaduzovic-Hadziabdic, Kanita, Hellemans, Jan, Heymans, Stephane, Hlavackova, Markéta, Hoydal, Morten Andre, Jankovic, Aleksandra, Jusic, Amela, Kardassis, Dimitris, Kerkelä, Risto, Kuster, Gabriela M., Lakkisto, Päivi, Leszek, Przemyslaw, Lustrek, Mitja, Maegdefessel, Lars, Martelli, Fabio, Novella, Susana, O’Brien, Timothy, Papaneophytou, Christos, Pedrazzini, Thierry, Pinet, Florence, Popescu, Octavian, Potočnjak, Ines, Robinson, Emma, Sasson, Shlomo, Scholz, Markus, Simionescu, Maya, Stoll, Monika, Varga, Zoltan V., Vinciguerra, Manlio, Xuereb, Angela, Yilmaz, Mehmet Birhan, Emanueli, Costanza, and Devaux, Yvan

Abstract

Cardiovascular disease (CVD) remains the leading cause of death worldwide and, despite continuous advances, better diagnostic and prognostic tools, as well as therapy, are needed. The human transcriptome, which is the set of all RNA produced in a cell, is much more complex than previously thought and the lack of dialogue between researchers and industrials and consensus on guidelines to generate data make it harder to compare and reproduce results. This European Cooperation in Science and Technology (COST) Action aims to accelerate the understanding of transcriptomics in CVD and further the translation of experimental data into usable applications to improve personalized medicine in this field by creating an interdisciplinary network. It aims to provide opportunities for collaboration between stakeholders from complementary backgrounds, allowing the functions of different RNAs and their interactions to be more rapidly deciphered in the cardiovascular context for translation into the clinic, thus fostering personalized medicine and meeting a current public health challenge. Thus, this Action will advance studies on cardiovascular transcriptomics, generate innovative projects, and consolidate the leadership of European research groups in the field. COST (European Cooperation in Science and Technology) is a funding organization for research and innovation networks (www.cost.eu).

Published
2019

41. Membrane glycoprotein PC-1 and insulin resistance in non-insulin-dependent diabetes mellitus

Author

Maddux, Betty A., Sbraccia, Paolo, Kumakura, Shinobu, Sasson, Shlomo, Youngren, Jack, Fisher, Alexander, Spencer, Steven, Grupe, Andrew, Henzel, William, and Stewart, Timothy A.

Subjects
Diabetes -- Research, Insulin resistance -- Analysis, Glycoproteins -- Research, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Analysis of an inhibitor of insulin-receptor tyrosine kinase, which is present in skin fibroblasts of insulin-resistant patients, reveals it as a membrane glycoprotein, PC-1. Out of nine patients with non-insulin-dependent diabetes mellitus, seven patients have significant PC-1 activity in fibroblasts. Insulin-induced tyrosine kinase activity is decreased by the overexpression of PC-1 in transfected cultured cells, suggesting the vital role of PC-1 in the insulin-resistance of non-insulin-dependent diabetes mellitus.

Published
1995

42. Insulin activates furosemide-sensitive K+ and Cl- uptake system in BC3H1 cells

Author

Weil-Maslansky, Evelyne, Gutman, Yehuda, and Sasson, Shlomo

Subjects
Musculoskeletal system -- Research, Insulin -- Physiological aspects, Biological transport -- Research, Biological sciences
Abstract

Measurements of the bumetanide- and furosemide-inhibitable 86Rb+ uptake in the skeletal muscle-like BC3 H1 cell lines reveal that insulin-like growth factor I (IGF-I) and insulin stimulate a loop diuretic-sensitive K+ and Cl- uptake system that depends on extracellular Cl- levels and is independent of extracellular Na+ levels. The K+-Cl- cotransport system is sensitive to furosemide and is kinetically distinct from the K+-Cl- cotransporters of other cells. Activation of the K+-Cl- cotransport system disappears without extracellular Cl- levels.

Published
1994

48. Catalyzing Transcriptomics Research in Cardiovascular Disease: The CardioRNA COST Action CA17129

Author

Gomes, Clarissa, primary, Ágg, Bence, additional, Andova, Andrejaana, additional, Arslan, Serdal, additional, Baker, Andrew, additional, Barteková, Monika, additional, Beis, Dimitris, additional, Betsou, Fay, additional, Wettinger, Stephanie, additional, Bugarski, Branko, additional, Condorelli, Gianluigi, additional, Silva, Gustavo, additional, Danilin, Sabrina, additional, Gonzalo-Calvo, David, additional, Buil, Alfonso, additional, Carmo-Fonseca, Maria, additional, Enguita, Francisco, additional, Felekkis, Kyriacos, additional, Ferdinandy, Peter, additional, Gyöngyösi, Mariann, additional, Hackl, Matthias, additional, Karaduzovic-Hadziabdic, Kanita, additional, Hellemans, Jan, additional, Heymans, Stephane, additional, Hlavackova, Markéta, additional, Hoydal, Morten, additional, Jankovic, Aleksandra, additional, Jusic, Amela, additional, Kardassis, Dimitris, additional, Kerkelä, Risto, additional, Kuster, Gabriela, additional, Lakkisto, Päivi, additional, Leszek, Przemyslaw, additional, Lustrek, Mitja, additional, Maegdefessel, Lars, additional, Martelli, Fabio, additional, Novella, Susana, additional, O’Brien, Timothy, additional, Papaneophytou, Christos, additional, Pedrazzini, Thierry, additional, Pinet, Florence, additional, Popescu, Octavian, additional, Potočnjak, Ines, additional, Robinson, Emma, additional, Sasson, Shlomo, additional, Scholz, Markus, additional, Simionescu, Maya, additional, Stoll, Monika, additional, Varga, Zoltan, additional, Vinciguerra, Manlio, additional, Xuereb, Angela, additional, Yilmaz, Mehmet, additional, Emanueli, Costanza, additional, Devaux, Yvan, additional, and EU-CardioRNA COST Action (CAonesevenonetwonine), on behalf of the, additional

Published
2019
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50. Endothelial Cell–Derived Triosephosphate Isomerase Attenuates Insulin Secretion From Pancreatic Beta Cells of Male Rats.

Author

Daniel, Bareket, Livne, Ariela, Cohen, Guy, Kahremany, Shirin, and Sasson, Shlomo

Subjects
PANCREATIC beta cells, TRIOSE-phosphate isomerase, PANCREATIC secretions, ISLANDS of Langerhans, INSULIN
Abstract

Insulin secretion from pancreatic beta cells is tightly regulated by glucose and paracrine signals within the microenvironment of islets of Langerhans. Extracellular matrix from islet microcapillary endothelial cells (IMEC) affect beta-cell spreading and amplify insulin secretion. This study was aimed at investigating the hypothesis that contact-independent paracrine signals generated from IMEC may also modulate beta-cell insulin secretory functions. For this purpose, conditioned medium (CMp) preparations were prepared from primary cultures of rat IMEC and were used to simulate contact-independent beta cell–endothelial cell communication. Glucose-stimulated insulin secretion (GSIS) assays were then performed on freshly isolated rat islets and the INS-1E insulinoma cell line, followed by fractionation of the CMp, mass spectroscopic identification of the factor, and characterization of the mechanism of action. The IMEC-derived CMp markedly attenuated first- and second-phase GSIS in a time- and dose-dependent manner without altering cellular insulin content and cell viability. Size exclusion fractionation, chromatographic and mass-spectroscopic analyses of the CMp identified the attenuating factor as the enzyme triosephosphate isomerase (TPI). An antibody against TPI abrogated the attenuating activity of the CMp while recombinant human TPI (hTPI) attenuated GSIS from beta cells. This effect was reversed in the presence of tolbutamide in the GSIS assay. In silico docking simulation identified regions on the TPI dimer that were important for potential interactions with the extracellular epitopes of the sulfonylurea receptor in the complex. This study supports the hypothesis that an effective paracrine interaction exists between IMEC and beta cells and modulates glucose-induced insulin secretion via TPI–sulfonylurea receptor–KATP channel (SUR1-Kir6.2) complex attenuating interactions. [ABSTRACT FROM AUTHOR]

Published
2021
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