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9. 122 - Temporal deletions of Nkx2-5 induce hypertrabeculation and progressive conduction defects and heart failure

Author

Nguyen, M., Choquet, C., Sicard, Pierre, Kober, F., Varlet, I., Rihet, P., Richard, Sylvain, Nguyen, C., Bernard, M., Kelly, R., Lalevee, N., Miquerol, L., Aix Marseille Université (AMU), Physiologie & médecine expérimentale du Cœur et des Muscles [U 1046] (PhyMedExp), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Centre de résonance magnétique biologique et médicale (CRMBM), Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-Centre National de la Recherche Scientifique (CNRS), Technologies avancées pour le génôme et la clinique (TAGC), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut de recherches sur la catalyse et l'environnement de Lyon (IRCELYON), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut de Chimie du CNRS (INC)-Centre National de la Recherche Scientifique (CNRS), Université de Montpellier (UM)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Assistance Publique - Hôpitaux de Marseille (APHM)-Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), and Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC)

Subjects
[SDV.IB.IMA]Life Sciences [q-bio]/Bioengineering/Imaging, [INFO.INFO-IM]Computer Science [cs]/Medical Imaging, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2017
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12. Deletion of Nkx2-5 in trabecular myocardium reveals the developmental origins of pathological heterogeneity associated with ventricular non-compaction cardiomyopathy

Author

Choquet, C, Nguyen, THM, Sicard, P, Buttigieg, E, Tran, TT, Kober, F, Varlet, I, Sturny, R, Costa, MW, Harvey, RP, Nguyen, C, Rihet, P, Richard, S, Bernard, M, Kelly, RG, Lalevée, N, Miquerol, L, Choquet, C, Nguyen, THM, Sicard, P, Buttigieg, E, Tran, TT, Kober, F, Varlet, I, Sturny, R, Costa, MW, Harvey, RP, Nguyen, C, Rihet, P, Richard, S, Bernard, M, Kelly, RG, Lalevée, N, and Miquerol, L

Abstract

Left ventricular non-compaction (LVNC) is a rare cardiomyopathy associated with a hypertrabeculated phenotype and a large spectrum of symptoms. It is still unclear whether LVNC results from a defect of ventricular trabeculae development and the mechanistic basis that underlies the varying severity of this pathology is unknown. To investigate these issues, we inactivated the cardiac transcription factor Nkx2-5 in trabecular myocardium at different stages of trabecular morphogenesis using an inducible Cx40-creERT2 allele. Conditional deletion of Nkx2-5 at embryonic stages, during trabecular formation, provokes a severe hypertrabeculated phenotype associated with subendocardial fibrosis and Purkinje fiber hypoplasia. A milder phenotype was observed after Nkx2-5 deletion at fetal stages, during trabecular compaction. A longitudinal study of cardiac function in adult Nkx2-5 conditional mutant mice demonstrates that excessive trabeculation is associated with complex ventricular conduction defects, progressively leading to strain defects, and, in 50% of mutant mice, to heart failure. Progressive impaired cardiac function correlates with conduction and strain defects independently of the degree of hypertrabeculation. Transcriptomic analysis of molecular pathways reflects myocardial remodeling with a larger number of differentially expressed genes in the severe versus mild phenotype and identifies Six1 as being upregulated in hypertrabeculated hearts. Our results provide insights into the etiology of LVNC and link its pathogenicity with compromised trabecular development including compaction defects and ventricular conduction system hypoplasia.

Published
2018

13. 14-3-3epsilon controls multiple developmental processes in the mouse heart

Author

Gittenberger-de Groot, A.C., Hoppenbrouwers, T., Miquerol, L., Kosaka, Y., Poelmann, R.E., Wisse, L.J., Yost, H.J., Jongbloed, M.R.M., Deruiter, M.C., Brunelli, L., Institut de Biologie du Développement de Marseille (IBDM), and Aix Marseille Université (AMU)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS)

Subjects
ventricular septal defect, coronary artery hypoplasia, endocardial cushion, cardiovascular system, cardiovascular diseases, heart development, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, myocardial hypoplasia, 14-3-3, mouse, cardiac outflow tract
Abstract

International audience; BACKGROUND:14-3-3ε plays an important role in the maturation of the compact ventricular myocardium by modulating the cardiomyocyte cell cycle via p27kip1 . However, additional cardiac defects are possible given the ubiquitous expression pattern of this protein.RESULTS:Germ line deletion of 14-3-3ε led to malalignment of both the outflow tract (OFT) and atrioventricular (AV) cushions, with resulting tricuspid stenosis and atresia, mitral valve abnormalities, and perimembranous ventricular septal defects (VSDs). We confirmed myocardial non-compaction and detected a spongy septum with muscular VSDs and blebbing of the epicardium. These defects were associated with abnormal patterning of p27kip1 expression in the subendocardial and possibly the epicardial cell populations. In addition to abnormal pharyngeal arch artery patterning, we found deep endocardial recesses and paucity of intramyocardial coronary vasculature as a result of defective coronary plexus remodeling.CONCLUSIONS:The malalignment of both endocardial cushions provides a new explanation for tricuspid and mitral valve defects, while myocardial non-compaction provides the basis for the abnormal coronary vasculature patterning. These abnormalities might arise from p27kip1 dysregulation and a resulting defect in epithelial-to-mesenchymal transformation. These data suggest that 14-3-3ε, in addition to left ventricular non-compaction (LVNC), might be linked to different forms of congenital heart disease (CHD). Developmental Dynamics 245:1107-1123, 2016. © 2016 Wiley Periodicals, Inc.

Published
2016
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14. Functional defects and molecular mechanisms of left ventricular non-compaction in nkx2.5 mutant mice

Author

Nguyen, T. H. M., Choquet, C., Kober, F., Monique BERNARD, Kelly, R. G., Miquerol, L., Lalevee, N., Mathématiques et Informatique pour la Complexité et les Systèmes (MICS), CentraleSupélec, Mutations des activités, des espaces et des formes d'organisation dans les territoires ruraux (METAFORT), Centre national du machinisme agricole, du génie rural, des eaux et forêts (CEMAGREF)-ENITA Clermont-AgroParisTech-Institut National de la Recherche Agronomique (INRA), Geological Institute, Eidgenössische Technische Hochschule - Swiss Federal Institute of Technology in Zürich [Zürich] (ETH Zürich), Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Collège de France (CdF)-Centre National de la Recherche Scientifique (CNRS), Technologies avancées pour le génôme et la clinique (TAGC), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Mutations des activités des espaces et des formes d'organisation dans les territoires ruraux (UMR METAFORT), Institut National de la Recherche Agronomique (INRA)-AgroParisTech-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Institut national de recherche en sciences et technologies pour l'environnement et l'agriculture (IRSTEA)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Centre de résonance magnétique biologique et médicale (CRMBM), Aix Marseille Université (AMU)-Assistance Publique - Hôpitaux de Marseille (APHM)-Centre National de la Recherche Scientifique (CNRS), Aix Marseille Université (AMU)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Recherche Agronomique (INRA)-AgroParisTech-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-Institut national de recherche en sciences et technologies pour l'environnement et l'agriculture (IRSTEA), and AgroParisTech-VetAgro Sup - Institut national d'enseignement supérieur et de recherche en alimentation, santé animale, sciences agronomiques et de l'environnement (VAS)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Institut National de la Recherche Agronomique (INRA)-Institut national de recherche en sciences et technologies pour l'environnement et l'agriculture (IRSTEA)

Subjects
[SDV]Life Sciences [q-bio]
Abstract

Frontiers in CardioVascular Biology Meeting (FCVB), Florence, ITALY, JUL 08-10, 2016; International audience; no abstract

Published
2016
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15. Coronary stem development in wild-type and Tbx1 null mouse hearts

Author

Théveniau-Ruissy, M., Pérez-Pomares, J.M., Parisot, P., Baldini, A., Miquerol, L., Kelly, R.G, Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS), Théveniau Ruissy, Magali, Pérez Pomares, José Maria, Parisot, Pauline, Baldini, Antonio, Miquerol, Lucile, and Kelly, Robert G.

Subjects
Stem Cells, Heart, Tbx1, Chick Embryo, heart development, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Coronary Vessels, Mice, Mutant Strains, Mice, cardiovascular system, Animals, Coronary arterie, coronary ostia, Endothelium, Vascular, T-Box Domain Proteins, coronary arteries, Aorta, Developmental Biology
Abstract

International audience; BACKGROUND:Coronary artery (CA) stems connect the ventricular coronary tree with the aorta. Defects in proximal CA patterning are a cause of sudden cardiac death. In mice lacking Tbx1, common arterial trunk is associated with an abnormal trajectory of the proximal left CA. Here we investigate CA stem development in wild-type and Tbx1 null embryos.RESULTS:Genetic lineage tracing reveals that limited outgrowth of aortic endothelium contributes to proximal CA stems. Immunohistochemistry and fluorescent tracer injections identify a periarterial vascular plexus present at the onset of CA stem development. Transplantation experiments in avian embryos indicate that the periarterial plexus originates in mesenchyme distal to the outflow tract. Tbx1 is required for the patterning but not timing of CA stem development and a Tbx1 reporter allele is expressed in myocardium adjacent to the left but not right CA stem. This expression domain is maintained in Sema3c(-/-) hearts with a common arterial trunk and leftward positioned CA. Ectopic myocardial differentiation is observed on the left side of the Tbx1(-/-) common arterial trunk.CONCLUSIONS:A periarterial plexus bridges limited outgrowth of the aortic endothelium with the ventricular plexus during CA stem development. Molecular differences associated with left and right CA stems provide new insights into the etiology of CA patterning defects.

Published
2016
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19. Young Investigator Award Session - Heart40Targeting the miRNA-106b-25 cluster as a potential regenerative therapeutic approach for myocardial injury41An allogeneic bioengineered myocardial graft limits infarct size and improves cardiac function: pre-clinical study in the porcine myocardial infarction model42Phosphoinositide 3-kinase gamma inhibition protects against anthracycline-induced cardiomyopathy by boosting cardiac autophagy43Functional screening of microRNAs identifies miR-22 as a regulator of cardiac autophagy and aging44Functional defects and molecular mechanisms of left ventricular non-compaction in nkx2.5 mutant mice45PITX2 modulates atrial membrane potential, potentiating the antiarrhythmic effects of sodium channel blockers

Author

Dirkx, E, primary, Perea Gil, I, primary, Li, MC, primary, Gupta, S K, primary, Nguyen, THM, primary, Syeda, F, primary, Dirkx, E, additional, Raso, A, additional, Braga, L, additional, Zentilin, L, additional, Zacchigna, S, additional, Giacca, M, additional, De Windt, LJ, additional, Prat-Vidal, C, additional, Galvez-Monton, C, additional, Roura, S, additional, Llucia-Valldeperas, A, additional, Soler-Botija, C, additional, Diaz-Guemes, I, additional, Crisostomo, V, additional, Sanchez-Margallo, FM, additional, Bayes-Genis, A, additional, Cimino, J, additional, De Santis, MC, additional, Pianca, N, additional, Sciarretta, S, additional, Sandri, M, additional, Zaglia, T, additional, Mongillo, M, additional, Hirsch, E, additional, Ghigo, A, additional, Bauters, C, additional, De Groote, P, additional, Foinquinos, A, additional, Boon, R, additional, Batkai, S, additional, Pinet, F, additional, Thum, T, additional, Choquet, C, additional, Kober, F, additional, Bernard, M, additional, Kelly, RG, additional, Miquerol, L, additional, Lalevee, N, additional, Holmes, A, additional, Yu, T, additional, Tull, S, additional, Kuhlmann, S, additional, Pavlovic, D, additional, Betney, D, additional, Riley, G, additional, Kucera, JP, additional, Jousset, F, additional, De Groot, J, additional, Rohr, S, additional, Brown, N, additional, Fabritz, L, additional, and Kirchhof, P, additional

Published
2016
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20. Thymosin beta4 facilitates epicardial neovascularization of the injured adult heart

Author

Smart, N, Risebro, C, Clark, J, Ehler, E, Miquerol, L, Rossdeutsch, A, Marber, MS, Riley, P, Institut de Biologie du Développement de Marseille (IBDM), and Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV.BC]Life Sciences [q-bio]/Cellular Biology, ComputingMilieux_MISCELLANEOUS
Abstract

Ischemic heart disease complicated by coronary artery occlusion causes myocardial infarction (MI), which is the major cause of morbidity and mortality in humans (http://www.who.int/cardiovascular_diseases/resources/atlas/en/index.html). After MI the human heart has an impaired capacity to regenerate and, despite the high prevalence of cardiovascular disease worldwide, there is currently only limited insight into how to stimulate repair of the injured adult heart from its component parts. Efficient cardiac regeneration requires the replacement of lost cardiomyocytes, formation of new coronary blood vessels, and appropriate modulation of inflammation to prevent maladaptive remodeling, fibrosis/scarring, and consequent cardiac dysfunction. Here we show that thymosin beta4 (Tbeta4) promotes new vasculature in both the intact and injured mammalian heart. We demonstrate that limited EPDC-derived endothelial-restricted neovascularization constitutes suboptimal "endogenous repair," following injury, which is significantly augmented by Tbeta4 to increase and stabilize the vascular plexus via collateral vessel growth. As such, we identify Tbeta4 as a facilitator of cardiac neovascularization and highlight adult EPDCs as resident progenitors which, when instructed by Tbeta4, have the capacity to sustain the myocardium after ischemic damage.

Published
2010

21. Gap junction protein Cx37 interacts with endothelial nitric oxide synthase in endothelial cells

Author

Pfenniger Anna, Derouette Jean-Paul, Verma Vandana, Lin Xianming, Foglia Bernard, Coombs Wanda, Roth Isabelle, Satta Nathalie, Dunoyer-Geindre Sylvie, Sorgen Paul, Taffet Steven, Kwak Brenda R, Delmar Mario, Miquerol L, Deutsch U, Jongsma H J, Chanson M, and Kwak B R

Subjects
Patch-Clamp Techniques, Amino Acid Motifs, Plasma protein binding, 030204 cardiovascular system & hematology, Connexins, Membrane Potentials, chemistry.chemical_compound, Mice, 0302 clinical medicine, Enos, Connexins/genetics/*metabolism, Cross-Linking Reagents/chemistry, Cells, Cultured, ddc:616, 0303 health sciences, Nitric Oxide Synthase Type III, Transfection, Nitric oxide synthase, Endothelial stem cell, Cross-Linking Reagents, Biochemistry, Recombinant Fusion Proteins/metabolism, Cardiology and Cardiovascular Medicine, Protein Binding, Endothelial Cells/*enzymology, Recombinant Fusion Proteins, Nitric Oxide Synthase Type III/genetics/*metabolism, Biology, Nitric Oxide, Article, Nitric oxide, 03 medical and health sciences, Peptide Library, Animals, Humans, Immunoprecipitation, Binding site, 030304 developmental biology, Binding Sites, Polymorphism, Genetic, Endothelial Cells, Surface Plasmon Resonance, biology.organism_classification, Molecular biology, chemistry, Connexin 43, Nitric Oxide/metabolism, biology.protein, Connexin 43/metabolism
Abstract

Objective— The gap junction protein connexin37 (Cx37) plays an important role in cell-cell communication in the vasculature. A C1019T Cx37 gene polymorphism, encoding a P319S substitution in the regulatory C terminus of Cx37 (Cx37CT), correlates with arterial stenosis and myocardial infarction in humans. This study was designed to identify potential binding partners for Cx37CT and to determine whether the polymorphism modified this interaction. Methods and Results— Using a high-throughput phage display, we retrieved 2 binding motifs for Cx37CT: WHK … [K,R]XP … and FHK … [K,R]XXP … , the first being more common for Cx37CT-319P and the second more common for Cx37CT-319S. One of the peptides (WHRTPRLPPPVP) showed 77.7% homology with residues 843 to 854 of endothelial nitric oxide synthase (eNOS). In vitro binding of this peptide or of the homologous eNOS sequence to both Cx37CT isoforms was confirmed by cross-linking and surface plasmon resonance. Electrophysiological analysis of Cx37 single channel activity in transfected N2a cells showed that eNOS-like and eNOS(843–854) increased the frequency of events with conductances higher than 300 pS. We demonstrated that eNOS coimmunoprecipitated with Cx37 in a mouse endothelial cell (EC) line (bEnd.3), human primary ECs, and a human EC line transfected with Cx37-319P or Cx37-319S. Cx37 and eNOS colocalized at EC membranes. Moreover, a dose-dependent increase in nitric oxide production was observed in ECs treated with Cx37 antisense. Conclusion— Overall, our data show for the first time a functional and specific interaction between eNOS and Cx37. This interaction may be relevant for the control of vascular physiology both in health and in disease.

Published
2010

22. Monitoring clonal growth in the developing ventricle

Author

Miquerol, L., Kelly, R.G., Institut de Biologie du Développement de Marseille (IBDM), and Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV.BC]Life Sciences [q-bio]/Cellular Biology, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2009

24. Nkx2.5 cell-autonomous gene function is required for the postnatal formation of the peripheral Purkinje fiber network

Author

Meysen, S., Marger, L., Hewett, K.W., Jarry-Guichard, T., Agarcova, I., Chauvin, J.P., Perriard, J.C., Izumo, S., Gourdie, R.G., Mangoni, M., Nargeot, Joël, Gros, D., Miquerol, L., Institut de Biologie du Développement de Marseille (IBDM), and Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV.BC]Life Sciences [q-bio]/Cellular Biology, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2007

26. Discontinuous conduction in mouse bundle branches is caused by bundle-branch architecture

Author

van Veen, T. A., van Rijen, H. V., van Kempen, M. J., Miquerol, L., Opthof, T., Gros, D., Vos, M. A., Jongsma, H. J., de Bakker, J. M., Institut de Biologie du Développement de Marseille (IBDM), Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS), and Aix Marseille Université (AMU)-Collège de France (CdF (institution))-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV.BC]Life Sciences [q-bio]/Cellular Biology
Published
2005

27. Architectural and functional asymmetry of the His-Purkinje system of the murine heart

Author

Miquerol, L., Meysen, S., Mangoni, M., Bois, P., Van Rijen, H.V., Abran, P., Jongsma, H., Nargeot, Joël, Gros, D., Institut de Biologie du Développement de Marseille (IBDM), and Aix Marseille Université (AMU)-Centre National de la Recherche Scientifique (CNRS)

Subjects
[SDV.BC]Life Sciences [q-bio]/Cellular Biology
Published
2004

28. Endothelial-specific deletion of Connexin40 promotes atherosclerosis by increasing CD73-dependent leukocyte adhesion

Author

Chadjichristos, C.E., Scheckenbach, K.E.L., Veen, T.A.B. van, Richani Sarieddine, M.Z., Wit, C. de, Yang, Zhihong, Roth, I., Bacchetta, M., Viswambharan, Hema, Foglia, B., Dudez, T., Kempen, M.J.A. van, Coenjaerts, F.E.J., Miquerol, L., Deutsch, U., Jongsma, H.J., Chanson, M., Kwak, B.R., Chadjichristos, C.E., Scheckenbach, K.E.L., Veen, T.A.B. van, Richani Sarieddine, M.Z., Wit, C. de, Yang, Zhihong, Roth, I., Bacchetta, M., Viswambharan, Hema, Foglia, B., Dudez, T., Kempen, M.J.A. van, Coenjaerts, F.E.J., Miquerol, L., Deutsch, U., Jongsma, H.J., Chanson, M., and Kwak, B.R.

Abstract

Background— Endothelial dysfunction is the initiating event of atherosclerosis. The expression of connexin40 (Cx40), an endothelial gap junction protein, is decreased during atherogenesis. In the present report, we sought to determine whether Cx40 contributes to the development of the disease.Methods and Results— Mice with ubiquitous deletion of Cx40 are hypertensive, a risk factor for atherosclerosis. Consequently, we generated atherosclerosis-susceptible mice with endothelial-specific deletion of Cx40 (Cx40del mice). Cx40del mice were indeed not hypertensive. The progression of atherosclerosis was increased in Cx40del mice after 5 and 10 weeks of a high-cholesterol diet, and spontaneous lesions were observed in the aortic sinuses of young mice without such a diet. These lesions showed monocyte infiltration into the intima, increased expression of vascular cell adhesion molecule-1, and decreased expression of the ecto-enzyme CD73 in the endothelium. The proinflammatory phenotype of Cx40del mice was confirmed in another model of induced leukocyte recruitment from the lung microcirculation. Endothelial CD73 is known to induce antiadhesion signaling via the production of adenosine. We found that reducing Cx40 expression in vitro with small interfering RNA or antisense decreased CD73 expression and activity and increased leukocyte adhesion to mouse endothelial cells. These effects were reversed by an adenosine receptor agonist.Conclusions— Cx40-mediated gap junctional communication contributes to a quiescent nonactivated endothelium by propagating adenosine-evoked antiinflammatory signals between endothelial cells. Alteration in this mechanism by targeting Cx40 promotes leukocyte adhesion to the endothelium, thus accelerating atherosclerosis.

Published
2010

29. Poster session 3

Author

Nanka, O., primary, Krejci, E., additional, Pesevski, Z., additional, Sedmera, D., additional, Smart, N., additional, Rossdeutsch, A., additional, Dube, K. N., additional, Riegler, J., additional, Price, A. N., additional, Taylor, A., additional, Muthurangu, V., additional, Turner, M., additional, Lythgoe, M. F., additional, Riley, P. R., additional, Kryvorot, S., additional, Vladimirskaya, T., additional, Shved, I., additional, Schwarzl, M., additional, Seiler, S., additional, Huber, S., additional, Steendijk, P., additional, Maechler, H., additional, Truschnig-Wilders, M., additional, Pieske, B., additional, Post, H., additional, Caprio, C., additional, Baldini, A., additional, Chiavacci, E., additional, Dolfi, L., additional, Verduci, L., additional, Meghini, F., additional, Cremisi, F., additional, Pitto, L., additional, Kuan, T.-C., additional, Chen, M.-C., additional, Yang, T.-H., additional, Wu, W.-T., additional, Lin, C. S., additional, Rai, H., additional, Kumar, S., additional, Sharma, A. K., additional, Mastana, S., additional, Kapoor, A., additional, Pandey, C. M., additional, Agrawal, S., additional, Sinha, N., additional, Orlowska-Baranowska, E. H., additional, Placha, G., additional, Gora, J., additional, Baranowski, R., additional, Abramczuk, E., additional, Hryniewiecki, T., additional, Gaciong, Z., additional, Verschuren, J. J. W., additional, Wessels, J. A. M., additional, Trompet, S., additional, Stott, D. J., additional, Sattar, N., additional, Buckley, B., additional, Guchelaar, H. J., additional, Jukema, J. W., additional, Gharanei, M., additional, Hussain, A., additional, Mee, C. J., additional, Maddock, H. L., additional, Wijnen, W. J., additional, Van Den Oever, S., additional, Van Der Made, I., additional, Hiller, M., additional, Tijsen, A. J., additional, Pinto, Y. M., additional, Creemers, E. E., additional, Nikulina, S. U. Y., additional, Chernova, A., additional, Petry, A., additional, Rzymski, T., additional, Kracun, D., additional, Riess, F., additional, Pike, L., additional, Harris, A. L., additional, Gorlach, A., additional, Katare, R., additional, Oikawa, A., additional, Riu, F., additional, Beltrami, A. P., additional, Cesseli, D., additional, Emanueli, C., additional, Madeddu, P., additional, Zaglia, T., additional, Milan, G., additional, Franzoso, M., additional, Pesce, P., additional, Sarais, C., additional, Sandri, M., additional, Mongillo, M., additional, Butler, T. J., additional, Seymour, A.-M. L., additional, Ashford, D., additional, Jaffre, F., additional, Bussen, M., additional, Flohrschutz, I., additional, Martin, G. R., additional, Engelhardt, S., additional, Kararigas, G., additional, Nguyen, B. T., additional, Jarry, H., additional, Regitz-Zagrosek, V., additional, Van Bilsen, M., additional, Daniels, A., additional, Munts, C., additional, Janssen, B. J. A., additional, Van Der Vusse, G. J., additional, Van Nieuwenhoven, F. A., additional, Montalvo, C., additional, Villar, A. V., additional, Merino, D., additional, Garcia, R., additional, Llano, M., additional, Ares, M., additional, Hurle, M. A., additional, Nistal, J. F., additional, Dembinska-Kiec, A., additional, Beata Kiec-Wilk, B. K. W., additional, Anna Polus, A. P., additional, Urszula Czech, U. C., additional, Tatiana Konovaleva, T. K., additional, Gerd Schmitz, G. S., additional, Bertrand, L., additional, Balteau, M., additional, Timmermans, A., additional, Viollet, B., additional, Sakamoto, K., additional, Feron, O., additional, Horman, S., additional, Vanoverschelde, J. L., additional, Beauloye, C., additional, De Meester, C., additional, Martinez, E., additional, Martin, R., additional, Miana, M., additional, Jurado, R., additional, Gomez-Hurtado, N., additional, Bartolome, M. V., additional, San Roman, J. A., additional, Lahera, V., additional, Nieto, M. L., additional, Cachofeiro, V., additional, Rochais, F., additional, Sturny, R., additional, Mesbah, K., additional, Miquerol, L., additional, Kelly, R. G., additional, Messaoudi, S., additional, Gravez, B., additional, Tarjus, A., additional, Pelloux, V., additional, Samuel, J. L., additional, Delcayre, C., additional, Launay, J. M., additional, Clement, K., additional, Farman, N., additional, Jaisser, F., additional, Hadyanto, L., additional, Castellani, C., additional, Vescovo, G., additional, Ravara, B., additional, Tavano, R., additional, Pozzobon, M., additional, De Coppi, P., additional, Papini, E., additional, Vettor, R., additional, Thiene, G., additional, Angelini, A., additional, Meloni, M., additional, Caporali, A., additional, Cesselli, D., additional, Fortunato, O., additional, Avolio, E., additional, Schindler, R., additional, Simrick, S., additional, Brand, T., additional, Smart, N. S., additional, Herman, A., additional, Roura Ferrer, S., additional, Rodriguez Bago, J., additional, Soler-Botija, C., additional, Pujal, J. M., additional, Galvez-Monton, C., additional, Prat-Vidal, C., additional, Llucia-Valldeperas, A., additional, Blanco, J., additional, Bayes-Genis, A., additional, Foldes, G., additional, Maxime, M., additional, Ali, N. N., additional, Schneider, M. D., additional, Harding, S. E., additional, Reni, C., additional, Mangialardi, G., additional, De Pauw, A., additional, Sekkali, B., additional, Friart, A., additional, Ding, H., additional, Graffeuil, A., additional, Catalucci, D., additional, Balligand, J. 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Published
2012
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31. Endothelial-Specific Deletion of Connexin40 Promotes Atherosclerosis by Increasing CD73-Dependent Leukocyte Adhesion

Author

Chadjichristos, C.E., primary, Scheckenbach, K.E.L., additional, van Veen, T.A.B., additional, Richani Sarieddine, M.Z., additional, de Wit, C., additional, Yang, Z., additional, Roth, I., additional, Bacchetta, M., additional, Viswambharan, H., additional, Foglia, B., additional, Dudez, T., additional, van Kempen, M.J.A., additional, Coenjaerts, F.E.J., additional, Miquerol, L., additional, Deutsch, U., additional, Jongsma, H.J., additional, Chanson, M., additional, and Kwak, B.R., additional

Published
2010
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39. Identification and functional characterization of an erythroid-specific enhancer in the L-type pyruvate kinase gene.

Author

Lacronique, V, Lopez, S, Miquerol, L, Porteu, A, Kahn, A, and Raymondjean, M

Abstract

The rat L-type pyruvate kinase gene is transcribed either from promoter L in the liver or promoter L' in erythroid cells. We have now cloned and functionally characterized an erythroid-specific enhancer, mapped in the fetal liver as hypersensitive site B (HSSB) at 3.7 kilobases upstream from the promoter L'. Protein-DNA interactions were examined in the 200-base pair core of the site by in vivo footprinting experiments. In the fetal liver, footprints were revealed at multiple GATA and CACC/GT motifs, whose association is the hallmark of erythroid-specific regulatory sequences. Functional analysis of the HSSB element in transgenic mice revealed properties of a cell-restricted enhancer. Indeed, this element was able to activate the linked ubiquitous herpes simplex virus thymidine kinase promoter in erythroid tissues. The activation was also observed in a variety of nonerythroid tissues known to synthesize GATA-binding factors. In the context of L'-PK transgenes, HSSB was not needed for an erythroid-specific activation of the L' promoter, while it was required to stimulate the L' promoter activity to a proper level. Finally, HSSB cannot be replaced by strong ubiquitous viral or cellular enhancers, suggesting a preferential interaction of the HSSB region with the L' promoter.

Published
1995

41. Endothelial-specific deletion of Connexin40 promotes atherosclerosis by increasing CD73-dependent leukocyte adhesion

Author

Chadjichristos, C.E., Scheckenbach, K.E.L., Veen, T.A.B. van, Richani Sarieddine, M.Z., Wit, C. de, Yang, Zhihong, Roth, I., Bacchetta, M., Viswambharan, Hema, Foglia, B., Dudez, T., Kempen, M.J.A. van, Coenjaerts, F.E.J., Miquerol, L., Deutsch, U., Jongsma, H.J., Chanson, M., Kwak, B.R., Chadjichristos, C.E., Scheckenbach, K.E.L., Veen, T.A.B. van, Richani Sarieddine, M.Z., Wit, C. de, Yang, Zhihong, Roth, I., Bacchetta, M., Viswambharan, Hema, Foglia, B., Dudez, T., Kempen, M.J.A. van, Coenjaerts, F.E.J., Miquerol, L., Deutsch, U., Jongsma, H.J., Chanson, M., and Kwak, B.R.

Abstract

Background— Endothelial dysfunction is the initiating event of atherosclerosis. The expression of connexin40 (Cx40), an endothelial gap junction protein, is decreased during atherogenesis. In the present report, we sought to determine whether Cx40 contributes to the development of the disease.Methods and Results— Mice with ubiquitous deletion of Cx40 are hypertensive, a risk factor for atherosclerosis. Consequently, we generated atherosclerosis-susceptible mice with endothelial-specific deletion of Cx40 (Cx40del mice). Cx40del mice were indeed not hypertensive. The progression of atherosclerosis was increased in Cx40del mice after 5 and 10 weeks of a high-cholesterol diet, and spontaneous lesions were observed in the aortic sinuses of young mice without such a diet. These lesions showed monocyte infiltration into the intima, increased expression of vascular cell adhesion molecule-1, and decreased expression of the ecto-enzyme CD73 in the endothelium. The proinflammatory phenotype of Cx40del mice was confirmed in another model of induced leukocyte recruitment from the lung microcirculation. Endothelial CD73 is known to induce antiadhesion signaling via the production of adenosine. We found that reducing Cx40 expression in vitro with small interfering RNA or antisense decreased CD73 expression and activity and increased leukocyte adhesion to mouse endothelial cells. These effects were reversed by an adenosine receptor agonist.Conclusions— Cx40-mediated gap junctional communication contributes to a quiescent nonactivated endothelium by propagating adenosine-evoked antiinflammatory signals between endothelial cells. Alteration in this mechanism by targeting Cx40 promotes leukocyte adhesion to the endothelium, thus accelerating atherosclerosis.

43. Transient formation of collaterals contributes to the restoration of the arterial tree during cardiac regeneration in neonatal mice.

Author

Sturny R, Boulgakoff L, Kelly RG, and Miquerol L

Subjects
Animals, Mice, Heart physiology, Neovascularization, Physiologic, Myocardium pathology, Myocardium metabolism, Disease Models, Animal, Regeneration, Animals, Newborn, Coronary Vessels, Collateral Circulation physiology, Myocardial Infarction physiopathology, Myocardial Infarction pathology
Abstract

Revascularization of ischemic myocardium following cardiac damage is an important step in cardiac regeneration. However, the mechanism of arteriogenesis has not been well described during cardiac regeneration. Here we investigated coronary artery remodeling and collateral growth during cardiac regeneration. Neonatal MI was induced by ligature of the left descending artery (LAD) in postnatal day (P) 1 or P7 pups from the Cx40-GFP mouse line and the arterial tree was reconstructed in 3D from images of cleared hearts collected at 1, 2, 4, 7 and 14 days after infarction. We show a rapid remodeling of the left coronary arterial tree induced by neonatal MI and the formation of numerous collateral arteries, which are transient in regenerating hearts after MI at P1 and persistent in non-regenerating hearts after MI at P7. This difference is accompanied by restoration of a perfused or a non-perfused LAD following MI at P1 or P7 respectively. Interestingly, collaterals ameliorate cardiac perfusion and drive LAD repair, and lineage tracing analysis demonstrates that the restoration of the LAD occurs by remodeling of pre-existing arterial cells independently of whether they originate in large arteries or arterioles. These results demonstrate that the restoration of the LAD artery during cardiac regeneration occurs by pruning as the rapidly forming collaterals that support perfusion of the disconnected lower LAD subsequently disappear on restoration of a unique LAD. These results highlight a rapid phase of arterial remodeling that plays an important role in vascular repair during cardiac regeneration., (Copyright © 2024 Elsevier Ltd. All rights reserved.)

Published
2024
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45. Participation of ventricular trabeculae in neonatal cardiac regeneration leads to ectopic recruitment of Purkinje-like cells.

Author

Boulgakoff L, Sturny R, Olejnickova V, Sedmera D, Kelly RG, and Miquerol L

Subjects
Animals, Cell Proliferation, Hyperplasia pathology, Myocytes, Cardiac pathology, Myocytes, Cardiac physiology, Cell Lineage, Mice, Mice, Transgenic, Regeneration physiology, Animals, Newborn, Heart Ventricles pathology, Heart Ventricles physiopathology, Purkinje Fibers physiopathology, Purkinje Fibers physiology, Purkinje Fibers pathology
Abstract

Unlike adult mammals, newborn mice can regenerate a functional heart after myocardial infarction; however, the precise origin of the newly formed cardiomyocytes and whether the distal part of the conduction system (the Purkinje fiber (PF) network) is properly formed in regenerated hearts remains unclear. PFs, as well as subendocardial contractile cardiomyocytes, are derived from trabeculae, transient myocardial ridges on the inner ventricular surface. Here, using connexin 40-driven genetic tracing, we uncover a substantial participation of the trabecular lineage in myocardial regeneration through dedifferentiation and proliferation. Concomitantly, regeneration disrupted PF network maturation, resulting in permanent PF hyperplasia and impaired ventricular conduction. Proliferation assays, genetic impairment of PF recruitment, lineage tracing and clonal analysis revealed that PF network hyperplasia results from excessive recruitment of PFs due to increased trabecular fate plasticity. These data indicate that PF network hyperplasia is a consequence of trabeculae participation in myocardial regeneration., (© 2024. The Author(s), under exclusive licence to Springer Nature Limited.)

Published
2024
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46. Molecular Regulation of Cardiac Conduction System Development.

Author

Boulgakoff L, D'Amato G, and Miquerol L

Subjects
Animals, Humans, Arrhythmias, Cardiac physiopathology, Mice, Gene Expression Regulation, Developmental, Cell Differentiation, Morphogenesis, Gene Regulatory Networks, Heart Conduction System physiopathology, Myocytes, Cardiac physiology
Abstract

Purpose of Review: The cardiac conduction system, composed of pacemaker cells and conducting cardiomyocytes, orchestrates the propagation of electrical activity to synchronize heartbeats. The conduction system plays a crucial role in the development of cardiac arrhythmias. In the embryo, the cells of the conduction system derive from the same cardiac progenitors as the contractile cardiomyocytes and and the key question is how this choice is made during development., Recent Findings: This review focuses on recent advances in developmental biology using the mouse as animal model to better understand the cellular origin and molecular regulations that control morphogenesis of the cardiac conduction system, including the latest findings in single-cell transcriptomics. The conducting cell fate is acquired during development starting with pacemaking activity and last with the formation of a complex fast-conducting network. Cardiac conduction system morphogenesis is controlled by complex transcriptional and gene regulatory networks that differ in the components of the cardiac conduction system., (© 2024. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.)

Published
2024
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47. Lineage-tracing hematopoietic stem cell origins in vivo to efficiently make human HLF+ HOXA+ hematopoietic progenitors from pluripotent stem cells.

Author

Fowler JL, Zheng SL, Nguyen A, Chen A, Xiong X, Chai T, Chen JY, Karigane D, Banuelos AM, Niizuma K, Kayamori K, Nishimura T, Cromer MK, Gonzalez-Perez D, Mason C, Liu DD, Yilmaz L, Miquerol L, Porteus MH, Luca VC, Majeti R, Nakauchi H, Red-Horse K, Weissman IL, Ang LT, and Loh KM

Subjects
Animals, Humans, Mice, Endothelial Cells metabolism, Endothelial Cells cytology, Hematopoiesis, Homeodomain Proteins metabolism, Homeodomain Proteins genetics, Transcription Factors metabolism, Transcription Factors genetics, Basic-Leucine Zipper Transcription Factors genetics, Basic-Leucine Zipper Transcription Factors metabolism, Cell Differentiation, Cell Lineage, Hematopoietic Stem Cells metabolism, Hematopoietic Stem Cells cytology, Pluripotent Stem Cells metabolism, Pluripotent Stem Cells cytology
Abstract

The developmental origin of blood-forming hematopoietic stem cells (HSCs) is a longstanding question. Here, our non-invasive genetic lineage tracing in mouse embryos pinpoints that artery endothelial cells generate HSCs. Arteries are transiently competent to generate HSCs for 2.5 days (∼E8.5-E11) but subsequently cease, delimiting a narrow time frame for HSC formation in vivo. Guided by the arterial origins of blood, we efficiently and rapidly differentiate human pluripotent stem cells (hPSCs) into posterior primitive streak, lateral mesoderm, artery endothelium, hemogenic endothelium, and >90% pure hematopoietic progenitors within 10 days. hPSC-derived hematopoietic progenitors generate T, B, NK, erythroid, and myeloid cells in vitro and, critically, express hallmark HSC transcription factors HLF and HOXA5-HOXA10, which were previously challenging to upregulate. We differentiated hPSCs into highly enriched HLF+ HOXA+ hematopoietic progenitors with near-stoichiometric efficiency by blocking formation of unwanted lineages at each differentiation step. hPSC-derived HLF+ HOXA+ hematopoietic progenitors could avail both basic research and cellular therapies., Competing Interests: Declaration of interests Stanford University has filed patent applications related to blood and immune cell differentiation. J.L.F. is presently at Walking Fish Therapeutics, A.C. is presently at Orca Bio, and T.N. is presently at Century Therapeutics, but J.L.F., A.C., and T.N. contributed to this work while they were at Stanford University; none of these companies were involved in the present work., (Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)

Published
2024
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48. Complementary and Inducible creER T2 Mouse Models for Functional Evaluation of Endothelial Cell Subtypes in the Bone Marrow.

Author

Poulos MG, Ramalingam P, Winiarski A, Gutkin MC, Katsnelson L, Carter C, Pibouin-Fragner L, Eichmann A, Thomas JL, Miquerol L, and Butler JM

Subjects
Animals, Mice, Bone Marrow metabolism, Mice, Transgenic, Bone Marrow Cells metabolism, Bone Marrow Cells cytology, Hematopoietic Stem Cells metabolism, Hematopoietic Stem Cells cytology, Hematopoiesis, Endothelial Cells metabolism, Integrases metabolism, Integrases genetics, Tamoxifen pharmacology
Abstract

In the adult bone marrow (BM), endothelial cells (ECs) are an integral component of the hematopoietic stem cell (HSC)-supportive niche, which modulates HSC activity by producing secreted and membrane-bound paracrine signals. Within the BM, distinct vascular arteriole, transitional, and sinusoidal EC subtypes display unique paracrine expression profiles and create anatomically-discrete microenvironments. However, the relative contributions of vascular endothelial subtypes in supporting hematopoiesis is unclear. Moreover, constitutive expression and off-target activity of currently available endothelial-specific and endothelial-subtype-specific murine cre lines potentially confound data analysis and interpretation. To address this, we describe two tamoxifen-inducible cre-expressing lines, Vegfr3-creER T2 and Cx40-creER T2 , that efficiently label sinusoidal/transitional and arteriole endothelium respectively in adult marrow, without off-target activity in hematopoietic or perivascular cells. Utilizing an established mouse model in which cre-dependent recombination constitutively-activates MAPK signaling within adult endothelium, we identify arteriole ECs as the driver of MAPK-mediated hematopoietic dysfunction. These results define complementary tamoxifen-inducible creER T2 -expressing mouse lines that label functionally-discrete and non-overlapping sinusoidal/transitional and arteriole EC populations in the adult BM, providing a robust toolset to investigate the differential contributions of vascular subtypes in maintaining hematopoietic homeostasis., (© 2024. The Author(s).)

Published
2024
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49. Dbh + catecholaminergic cardiomyocytes contribute to the structure and function of the cardiac conduction system in murine heart.

Author

Sun T, Grassam-Rowe A, Pu Z, Li Y, Ren H, An Y, Guo X, Hu W, Liu Y, Zheng Y, Liu Z, Kou K, Ou X, Chen T, Fan X, Liu Y, Tu S, He Y, Ren Y, Chen A, Shang Z, Xia Z, Miquerol L, Smart N, Zhang H, Tan X, Shou W, and Lei M

Subjects
Mice, Animals, Heart Conduction System, Mammals, Gene Expression Profiling, Dopamine beta-Hydroxylase, Myocytes, Cardiac, Heart physiology
Abstract

The heterogeneity of functional cardiomyocytes arises during heart development, which is essential to the complex and highly coordinated cardiac physiological function. Yet the biological and physiological identities and the origin of the specialized cardiomyocyte populations have not been fully comprehended. Here we report a previously unrecognised population of cardiomyocytes expressing Dbhgene encoding dopamine beta-hydroxylase in murine heart. We determined how these myocytes are distributed across the heart by utilising advanced single-cell and spatial transcriptomic analyses, genetic fate mapping and molecular imaging with computational reconstruction. We demonstrated that they form the key functional components of the cardiac conduction system by using optogenetic electrophysiology and conditional cardiomyocyte Dbh gene deletion models. We revealed their close relationship with sympathetic innervation during cardiac conduction system formation. Our study thus provides new insights into the development and heterogeneity of the mammalian cardiac conduction system by revealing a new cardiomyocyte population with potential catecholaminergic endocrine function., (© 2023. The Author(s).)

Published
2023
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50. Optogenetic termination of atrial tachyarrhythmias by brief pulsed light stimulation.

Author

Nakao M, Watanabe M, Miquerol L, Natsui H, Koizumi T, Kadosaka T, Koya T, Hagiwara H, Kamada R, Temma T, de Vries AAF, and Anzai T

Subjects
Animals, Mice, Optogenetics methods, Channelrhodopsins genetics, Heart Atria, Tachycardia, Mice, Transgenic, Action Potentials, Atrial Fibrillation therapy
Abstract

Aims: The most efficient way to acutely restore sinus rhythm from atrial fibrillation (AF) is electrical cardioversion, which is painful without adequate sedation. Recent studies in various experimental models have indicated that optogenetic termination of AF using light-gated ion channels may provide a myocardium-specific and potentially painless alternative future therapy. However, its underlying mechanism(s) remain(s) incompletely understood. As brief pulsed light stimulation, even without global illumination, can achieve optogenetic AF termination, besides direct conduction block also modulation of action potential (AP) properties may be involved in the termination mechanism. We studied the relationship between optogenetic AP duration (APD) and effective refractory period (ERP) prolongation by brief pulsed light stimulation and termination of atrial tachyarrhythmia (AT)., Methods and Results: Hearts from transgenic mice expressing the H134R variant of channelrhodopsin-2 in atrial myocytes were explanted and perfused retrogradely. AT induced by electrical stimulation was terminated by brief pulsed blue light stimulation (470 nm, 10 ms, 16 mW/mm 2 ) with 68% efficacy. The termination rate was dependent on pulse duration and light intensity. Optogenetically imposed APD and ERP changes were systematically examined and optically monitored. Brief pulsed light stimulation (10 ms, 6 mW/mm 2 ) consistently prolonged APD and ERP when light was applied at different phases of the cardiac action potential. Optical tracing showed light-induced APD prolongation during the termination of AT., Conclusion: Our results directly demonstrate that cationic channelrhodopsin activation by brief pulsed light stimulation prolongs the atrial refractory period suggesting that this is one of the key mechanisms of optogenetic termination of AT., Competing Interests: Declaration of Competing Interest None declared., (Copyright © 2023. Published by Elsevier Ltd.)

Published
2023
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