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Littérature scientifique sur le sujet « Cardiogenesi »

Auteur : Grafiati
Publié le 9 mars 2023
Mis à jour le 10 mars 2023

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Articles de revues sur le sujet "Cardiogenesi"

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Nascone, Nanette, et Mark Mercola. « Endoderm and Cardiogenesis ». Trends in Cardiovascular Medicine 6, no 7 (octobre 1996) : 211–16. http://dx.doi.org/10.1016/s1050-1738(96)00086-2.

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Samuel, L. J., et B. V. Latinkic. « MHC and cardiogenesis ». Development 137, no 1 (18 décembre 2009) : 3. http://dx.doi.org/10.1242/dev.044917.

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Martin, James F., Emerson C. Perin et James T. Willerson. « Direct Stimulation of Cardiogenesis ». Circulation Research 121, no 1 (23 juin 2017) : 13–15. http://dx.doi.org/10.1161/circresaha.117.311062.

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Metzger, Joseph M., Linda C. Samuelson, Elizabeth M. Rust et Margaret V. Westfall. « Embryonic Stem Cell Cardiogenesis ». Trends in Cardiovascular Medicine 7, no 2 (février 1997) : 63–68. http://dx.doi.org/10.1016/s1050-1738(96)00138-7.

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Sahara, Makoto, Elif Eroglu et Kenneth R. Chien. « Lnc’ed in to Cardiogenesis ». Cell Stem Cell 22, no 6 (juin 2018) : 787–89. http://dx.doi.org/10.1016/j.stem.2018.05.012.

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Muñoz-Chápuli, Ramón, et José M. Pérez-Pomares. « Cardiogenesis : An Embryological Perspective ». Journal of Cardiovascular Translational Research 3, no 1 (4 novembre 2009) : 37–48. http://dx.doi.org/10.1007/s12265-009-9146-1.

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Pucéat, Michel, et Marisa Jaconi. « Ca2+ signalling in cardiogenesis ». Cell Calcium 38, no 3-4 (septembre 2005) : 383–89. http://dx.doi.org/10.1016/j.ceca.2005.06.016.

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Li, Xing, Almudena Martinez-Fernandez, Katherine A. Hartjes, Jean-Pierre A. Kocher, Timothy M. Olson, Andre Terzic et Timothy J. Nelson. « Transcriptional atlas of cardiogenesis maps congenital heart disease interactome ». Physiological Genomics 46, no 13 (1 juillet 2014) : 482–95. http://dx.doi.org/10.1152/physiolgenomics.00015.2014.

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Mammalian heart development is built on highly conserved molecular mechanisms with polygenetic perturbations resulting in a spectrum of congenital heart diseases (CHD). However, knowledge of cardiogenic ontogeny that regulates proper cardiogenesis remains largely based on candidate-gene approaches. Mapping the dynamic transcriptional landscape of cardiogenesis from a genomic perspective is essential to integrate the knowledge of heart development into translational applications that accelerate disease discovery efforts toward mechanistic-based treatment strategies. Herein, we designed a time-course transcriptome analysis to investigate the genome-wide dynamic expression landscape of innate murine cardiogenesis ranging from embryonic stem cells to adult cardiac structures. This comprehensive analysis generated temporal and spatial expression profiles, revealed stage-specific gene functions, and mapped the dynamic transcriptome of cardiogenesis to curated pathways. Reconciling known genetic underpinnings of CHD, we deconstructed a disease-centric dynamic interactome encoded within this cardiogenic atlas to identify stage-specific developmental disturbances clustered on regulation of epithelial-to-mesenchymal transition (EMT), BMP signaling, NF-AT signaling, TGFb-dependent EMT, and Notch signaling. Collectively, this cardiogenic transcriptional landscape defines the time-dependent expression of cardiac ontogeny and prioritizes regulatory networks at the interface between health and disease.
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Mukhopadhyay, Madhura. « Recapitulating early cardiogenesis in vitro ». Nature Methods 18, no 4 (avril 2021) : 331. http://dx.doi.org/10.1038/s41592-021-01118-2.

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Brade, T., L. S. Pane, A. Moretti, K. R. Chien et K. L. Laugwitz. « Embryonic Heart Progenitors and Cardiogenesis ». Cold Spring Harbor Perspectives in Medicine 3, no 10 (1 octobre 2013) : a013847. http://dx.doi.org/10.1101/cshperspect.a013847.

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Thèses sur le sujet "Cardiogenesi"

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DI, MAURO VITTORIA. « Novel insights into the protective role of miR-133a in the heart and its therapeutic application for the treatment of cardiac pathologies ». Doctoral thesis, Università degli Studi di Milano-Bicocca, 2017. http://hdl.handle.net/10281/170792.

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Finora, diversi studi hanno dimostrato l'importanza dei miRNAs, in fase di sviluppo embrionale e nell’insorgenza di molte patologie. Nel sistema cardiaco, il ruolo del miR-133a è stato ampiamente caratterizzato dall’embriogenesi allo sviluppo di difetti cardiaci. Tuttavia, resta ancora molto da caratterizzare circa le funzioni del miR-133. Lo scopo principale della mia tesi di dottorato è stato indagare queste funzioni aggiuntive del miR-133 nello sviluppo cardiaco, in particolare sulla sua capacità di controllare vie di trasduzione a livello trascrizionale. La seconda fase della mia ricerca è stata quella approfondire il suo ruolo in patologie cardiache. In ultimo l'obiettivo finale della mia ricerca è stato quello di traslare l’importanza del miR-133 nel suo uso terapeutico con lo sviluppo di una nuova strategia che, basato sull'utilizzo dei nanomateriali al fine di sviluppare uno specifico e controllato rilascio di miR-133 nel sistema cardiovascolare.
So far, a plethora of studies demonstrated the importance of miRNAs, in embryo development and in the onset of basically all kinds of pathologies. In the cardiac system, the role of miR-133a was extensively characterized from embryogenesis to the development of cardiac defects. Nevertheless, much remains to be learned about the functions of miR-133. The main scope of my PhD thesis was to investigate these additional functions of miR-133 firstly in cardiac development, focusing on its potential ability to control signal pathways at the transcriptional level, and secondly in the already well characterized cardiac pathologies. Moreover, the ultimate goal of my research was to translate the additional roles of miR-133 into its therapeutic use by developing a new strategy that, based on the use of nanomaterials, allows for the specific and controlled delivery of miR-133 into the cardiac system.
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Potier, Delphine. « Approches in silico et in vivo pour l'étude de la régulation transcriptionnelle : application à la cardiogenèse chez D. melanogaster ». Thesis, Aix-Marseille 2, 2011. http://www.theses.fr/2011AIX22055.

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Au cours de ma thèse, je me suis intéressée au développement du système cardio-vasculaire chez la drosophile afin de mieux comprendre la logique de régulation de ce processus. Au cours de l'embryogenèse, la cardiogenèse est réalisée grâce à un réseau de régulation génique (GRN) qui conduit à la formation d'un simple tube cardiaque linéaire. Ensuite, lors de la métamorphose, le tube cardiaque larvaire est remodelé pour former l'organe adulte.J'ai d'abord participé à l'évaluation et à l'amélioration d'une nouvelle méthode, cisTargetX, qui permet prédire des modules cis-régulateurs (CRM) présentant des caractéristiques communes à un groupe de gènes co-exprimés.En utilisant cette méthode, j'ai analysé le transcriptome du remodelage du cœur afin de prédire des motifs pouvant être liés par des TF impliqués dans le contrôle temporel de l'expression des gènes, ainsi que les CRM associés. Grâce aux validations in-vivo des CRM prédits, j'ai démontré qu'ils étaient capables de reproduire le patron d'expression temporel attendu. J'ai également démontré que la mutation du motif en question au sein de deux des CRM testés permet de supprimer son patron d'expression sauvage. Ce motif est reconnu par des facteurs de transcription (TF) de la famille des récepteurs nucléaires (NR). Dhr3, un NR fortement exprimé au début de l'induction des gènes analysés, est montré comme étant essentiel au patron d'expression temporel. Nos résultats suggèrent une architecture du GRN, dans lequel les régulations temporelle et spatiale sont distinctes.Par la suite, j'ai participé à la caractérisation du GRN impliqué dans la cardiogenèse. En combinant un transcriptome issu de la différenciation des cellules cardiaques avec des expériences ChIP-on-Chip sur le TF MEF2, j'ai prédit que certains TF appartenant aux familles bZIP et REL sont susceptibles de participer au GRN responsable de la différenciation cardiaque. La validation in-vivo de ces prédictions est en cours
During my thesis, I focused on the development of the cardiovascular system in Drosophila in order to investigate the regulatory logic of this process. During embryogenesis, cardiogenesis is mediated by a gene regulatory network which includes conserved signaling pathways and transcription factors, and leads to the formation of a linear cardiac tube. Then, during metamorphosis, the larval cardiac tube is remodeled to form the adult organ.I first participated in the evaluation and the improvement of a new method, cisTargetX, that uses a comprehensive library of motifs, combined with phylogenetic conservation, to identify potential cis-regulatory modules (CRM) presenting common features in a cluster of co-expressed genes.Using this method among other tools, I analysed cardiac remodeling during metamorphosis to predict motifs for transcription factors (TF) involved in the temporal control of gene expression, and also their associated CRM. I performed in-vivo validations of predicted CRM, and demonstrated that they reproduce the expected temporal expression pattern. In addition, I demonstrated that motifs mutation within selected CRM abrogate this expression pattern. This motif is predicted to be recognized by a TF that belong to the nuclear receptor (NR) family. Dhr3, a NR highly expressed at the onset of the induction of the analysed gene set, is demonstrated to be essential for CRM temporal pattern. Our results suggest a modular architecture of the regulatory machinery, in which the temporal and spatial regulations are distinct.Next, I participated in the characterization of the Gene Regulatory Network (GRN) involved in cardiac differentiation during embryogenesis. Combining transcriptome profiling of differentiating cardiac cells with Mef2 Chip-on-Chip experiments allowed me to predict that TF belonging to bZIP and REL family are likely to participate in the GRN driving cardiac differentiation. In-vivo validation of these predictions is in progress
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Bobbs, Alexander Sebastian. « FGF Signaling During Gastrulation and Cardiogenesis ». Diss., The University of Arizona, 2012. http://hdl.handle.net/10150/265335.

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An early event in animal development is the formation of the three primary germ layers that define the body plan. During gastrulation, cells migrate through the primitive streak of the embryo and undergo changes in morphology and gene expression, thus creating the mesodermal and endodermal cell layers. Gastrulation requires expression of Fibroblast Growth Factor (FGF), Wnt, and Platelet-Derived Growth Factor (PDGF). Embryos treated with FGF inhibitors fail to gastrulate, as cell migration is completely halted. During gastrulation, 44 microRNAs are expressed in the primitive streak of G. gallus embryos, and six (microRNAs -let7b, -9, -19b, -107, -130b, and -218) are strongly upregulated when FGF signaling is blocked. The abundance of these six FGF-regulated microRNAs is controlled at various stages of processing: most are regulated transcriptionally, and three of them (let7b, 9, and 130b) are blocked by the presence of Lin28B, an RNA-binding protein upregulated by FGF signaling. These microRNAs target various serine/threonine and tyrosine kinase receptors. We propose a novel pathway by which FGF signaling downregulates several key microRNAs (partially through Lin28B), upregulating gene targets such as PDGFRA, which permits and directs cell migration during gastrulation. These findings add new layers of complexity to the role that FGF signaling plays during embryogenesis. FGF signaling is also required for the formation of the heartfields, and has an overlapping pattern of expression with BMP (Bone Morphogenetic Protein). A microarray experiment using inhibitors of FGF and BMP found that thousands of genes in pre-cardiac mesoderm are affected by FGF signaling, BMP signaling, or a cooperative effect of the two. The promoter regions of similarly regulated genes were queried for over-represented transcription factor binding sites or novel DNA motifs. Cluster analysis of over-represented sites determined candidate transcriptional modules that were tested in primary cardiac myocyte and fibroblast cultures. About 75% of predicted modules in FGF-upregulated genes proved to be functional enhancers or repressors. Functional enhancers among FGF-upregulated genes contained clusters of CdxA and NFY sites, and increased transcription in the presence of a constitutively active FGF receptor.
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Martin, Jennifer. « Wnt regulated transcription factor networks mediate vertebrate cardiogenesis ». Thesis, Available from the University of Aberdeen Library and Historic Collections Digital Resources. Online version available for University members only until Feb. 15, 2012, 2009. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?application=DIGITOOL-3&owner=resourcediscovery&custom_att_2=simple_viewer&pid=25801.

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Papoutsi, Tania. « Regulation of cardiogenesis by putative WNT signalling pathways ». Thesis, University of Newcastle Upon Tyne, 2011. http://hdl.handle.net/10443/1325.

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The Wnt/ -catenin and the Wnt/planar cell polarity (Wnt/PCP) signalling pathways have been shown to play important roles in cardiogenesis and their disruption has been shown to cause severe disturbances in heart development. Spatially and temporally complex interplays between the two pathways have been described. One component of the PCP pathway is Jnk, a member of the highly conserved mitogenactivated protein kinase (MAPK) family. This stress responsive mitogen is known to control a variety of cellular behaviours such as proliferation, apoptosis and cell migratory behaviour and as such, is likely to be of pivotal importance in cardiac development. The aim of this study was to investigate the role played by Jnk in vertebrate heart formation and the relationships between Jnk signalling and canonical Wnt signalling, using in silico and in vivo approaches in zebrafish and an in vitro approach on a mouse embryonic stem (ES) cell model of cardiogenesis. Firstly, using a range of bioinformatic methods, an analysis of jnk genes, splice variants and proteins, and an investigation of their phylogenetic relation with other species was undertaken. This suggested conservation of Jnk family members, but suggested that there were additional orthologues of jnk1 present in the zebrafish transcriptome. The spatial and temporal expression profiles of these genes were then examined by semi-quantitative PCR and in situ hybridisation. The functional role of Jnk proteins during zebrafish development was subsequently investigated using a specific chemical inhibitor, SP600125. Inhibition of Jnk signalling during gastrulation and somitogenesis caused a convergence extension-like phenotype and severe cardiac defects, including looping anomalies and alterations in atrial versus ventricular cell numbers. ES cells have the capacity to differentiate in vitro and give rise to cells of many different lineages, including cardiomyocytes. Canonical Wnt and Jnk components were manipulated during specific windows of differentiation as ES cells formed beating embryoid bodies. Examination of the spontaneous contractile behaviour of differentiating ES cells as they entered the cardiogenic lineage, and analysis of their developmental gene expression profiles, showed the beating behaviour of ES cellderived cardiac cells was enhanced in a temporally specific manner after inhibition of the non-canonical Wnt/Jnk pathway, while there was marked alteration of canonical Wnt signalling. To investigate whether there were reciprocal interactions between the two pathways, analysis of the system after activation of the canonical pathway was also undertaken. These studies indicated that the beating behaviour of ES cell-derived cardiac cells was enhanced in a temporally specific manner after inhibition of Jnk, while after activation of canonical Wnt/ -catenin signalling, the cardiogenic potential of differentiating ES cells was severely suppressed. The findings of this study extend our understanding of the role played by canonical and non-canonical Wnt signalling pathways in heart morphogenesis and highlight the interacting effects of related signalling pathways activity in cardiogenesis.
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Wan, Chen-rei. « Characterization of the cardiogenesis of embryonic stem cells ». Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/65283.

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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Mechanical Engineering, February 2011.
Cataloged from PDF version of thesis.
Includes bibliographical references (p. 114-127).
Cardiovascular diseases persist as the leading cause of mortality worldwide. Stem cell therapy, aimed to restore contractility and proper vasculature, has gained considerable attention as an attractive therapeutic option. However, proper cell differentiation, survival and integration in an infarcted zone remain elusive. This thesis aims to utilize in vitro techniques to obtain a systematic characterization of how individual stimulations can affect the cardiogenesis process of embryonic stem cells. First, a compliant microfluidic system was developed to study the individual and combined effects of culture dimensions and uniaxial cyclic stretch on the differentiation process. A smaller culture dimension, with a characteristic length scale of hundreds of micrometers, dramatically enhanced differentiation partly due to an accumulation of cell-secreted and cardiogenic BMP2. Uniaxial cyclic stretch, on the other hand, inhibited differentiation. With this microfluidic platform and a GFP-reporting differentiation cell line, effects of various external stimuli on differentiation were systematically studied. Next, the effects of collagen I and cell alignment, two biophysical signatures of the adult myocardium, on promoting phenotypic changes of isolated embryonic stem cell derived cardiomyocytes (ESCDMs) were investigated. Effects of collagen I depended on how it was presented to the cells and overlaying collagen gel impeded cell elongation. Binucleation. characteristic of maturing cardiomyocytes, was reduced with soluble collagen supplement and nanoscale topography and was associated with an increase in cytokinesis. Both nanoscale topography and microcontact printing resulted in aligned cardiomyocyte monolayers but produced different morphologies. Lastly, the lessons learned from studying the aforementioned processes were applied to test the utility of ESCDMs as biological actuators. Three proof-of-concept experiments were conducted: ESCDM monolayers were able to contract synchronously as a cell-assemble, force generated by the cell monolayer was estimated to be comparable to that by neonatal myocytes and lastly, the direction of contraction could be controlled with surface patterning. This work advances our understanding on the cardiogenic potential of murine embryonic stem cells and elucidated complex biological questions with well-characterized and controlled tissue engineering techniques.
by Chen-rei Wan.
Ph.D.
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Pang, Kar Lai. « The role of abnormal haemodynamics and cardiac troponin T in cardiogenesis ». Thesis, University of Nottingham, 2017. http://eprints.nottingham.ac.uk/39193/.

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The heart is the first functioning organ to develop during embryogenesis to maintain the growing embryo with oxygen and nutrients. However, cardiogenesis is a complex and highly coordinated biological process, and any perturbation to this process can result in detrimental defects to the heart. Haemodynamics is known to play an important role in cardiac growth and vasculature remodelling. Congenital heart defects (CHDs) accounts for 0.4-1.3% of all live birth, whereas cardiomyopathy accounts for 8-11% of cardiovascular disease diagnoses detected in utero. Although the heart defects and cardiomyopathies are known to be attributed by genetic mutations, most cases have unknown etiology. Hence, OFT-banding model was employed to alter the haemodynamic loading via pressure overloading. Upon alteration of haemodynamics, enlargement of the heart with a spectrum of cardiac anomalies were found (e.g ventricular septal defects, thickened epicardium and dysmorphic atrioventricular valves) upon morphological and stereological analysis. A study of global differential expression of OFT-banded hearts by RNA sequencing revealed a number of differentially expressed genes and they were associated with cardioprotection, metabolism, shear stress and valve development; further, a reduction of apoptosis was seen in these banded hearts as well. One of the cardiac phenotypes seen upon OFT-banding, the abnormal primordial atrioventricular valve, was further characterized to provide an insight how the atrioventricular valve is affected upon alteration of haemodynamics. Aberrant expressions of extracellular matrix (ECM) genes such as TBX20, Aggrecan and Periostin alongside with the shear stress responsive genes (KLF2 and EDN1) were found, and a decrease in apoptosis was seen. Moreover, dysregulation of ECM proteins such as fibrillin-2, type III collagen and tenascin were further demonstrated in more mature primordial AV leaflets at HH35, with a concomitant decrease of ECM cross-linking enzyme, transglutaminase-2. In addition, for many years sarcomeric proteins have been associated with a range of cardiomyopathies, but only in recent years they have been linked to congenital heart defects (CHDs). To date, cardiac troponin T (TNNT2) has been associated with cardiomyopathies but not with isolated CHDs. TNNT2 encodes for cTnT regulatory proteins of the thin filament of the sarcomere and is vital for muscle contraction and force generation within cardiomyocytes. To investigate a role of TNNT2 in the early developing heart, targeted manipulation of TNNT2 was performed in embryonic chick to reduce the protein levels of cTNT (protein product of TNNT2) in ovo via translational block. Abnormal atrial septal growth, reduced ventricular trabeculation and ventricular diverticula were found upon TNNT2 morpholino treatment. The abnormal phenotype observed in the TNNT2 morpholino-treated groups was potentially suggested by differential expression of shear stress responsive gene, NOS3 gene.
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Kriegeskotte, Dominik Matthias [Verfasser], et Friedhelm [Akademischer Betreuer] Beyersdorf. « Hämodynamische Veränderungen unter therapeutischer Hypothermie nach cardiogenem Schock ». Freiburg : Universität, 2011. http://d-nb.info/1123458804/34.

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Paiva, Solenne. « Facteurs environnementaux et épigénétiques impliqués dans la différenciation cardiaque de cellules souches humaines pluripotentes induites MiRroring the Multiple Potentials of MicroRNAs in Acute Myocardial Infarction Acellular therapeutic approach for heart failure : in vitro production of extracellular vesicles from human cardiovascular progenitors ». Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS457.

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L’objectif de cette thèse a été d’évaluer certains paramètres physiques et épigénétiques impliqués dans la différenciation cardiaque de cellules souches humaines pluripotentes induites. Un premier paramètre physique souvent sous-évalué a été étudié, celui de la rigidité. Classiquement, les cellules souches sont cultivées et adaptées à des rigidités in vitro allant de 1-10 GPa très éloignées des valeurs physiologiques, de l’ordre du kPa. L’impact de support de culture à 3, 12 et 25 kPa a été évalué sur les cellules souches initiales. Les résultats montrent que des rigidités inférieures à 25 kPa ne permettent pas le maintien de la pluripotence au bout de 6 passages. De plus, les colonies cellulaires se développent en 3D et créent leur propre microenvironnement. Un second paramètre étudié concerne les microRNAs appartenant à la famille let-7 dont la fonction exacte au niveau cardiaque reste à définir. Les résultats montrent qu’au cours de la différenciation son expression se caractérise par une augmentation transitoire précoce au moment de la formation du mésoderme, puis s’éteint pour ne ré-augmenter que plus tard lors de la maturation des cardiomyocytes. Des modulations via des mimics ou des inhibiteurs dans différents contextes cellulaires suggèrent qu’initialement let-7 contribue à une future spécification cardiaque, mais que plus tard cette famille devra être réprimée pour générer des progéniteurs cardiaques. À l’opposé, miR-1, spécifique au cœur, contribue toujours à la progression en cardiomyocytes. Ensemble, ces recherches contribuent à la recherche fondamentale sur le développement du cœur humain et à la recherche appliquée en ingénierie tissulaire cardiaque
The objective of this thesis was to evaluate some physical and epigenetic parameters involved during cardiac differentiation of human induced pluripotent stem cells. Environmentally, an often undervalued physical parameter remains, the stiffness defined by the Young’s modulus. Commonly stem cells are cultured and adapted to in vitro rigidities ranging between 1-10 GPa very far from physiological values, for instance 10-15 kPa for the heart. The impact of soft culture substrates with 3 kPa, 12 kPa and 25 kPa was studied on the initial stem cells. Globally, results indicated that rigidities lower than 25 kPa were not suited for total pluripotency maintenance after 6 passages. Also, cellular colonies started to grow in 3D suggesting that softness drove them to build their own microenvironment. Epigenetically, the exact role of one of the first discovered microRNAs, the let-7 family has not yet been fully elucidated. Throughout differentiation its expression was characterized by an early transient peak at the time of mesoderm formation, after which their expression extinguished to only gradually re-increase later in the course of cardiomyocytes maturation. Modulation experiments involving mimics or inhibitors of the let-7 family on different cellular contexts suggested that initially let-7 acted on future cardiac specification but later, this family had to be repressed in order for cardiac progenitors to emerge. Oppositely, the cardiac specific miR-1 always contributed to their progression into cardiomyocytes. Together these researches contribute to fundamental research on human heart development and to applied research on human engineered cardiac tissues
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Ridge, Liam. « Investigating the role of Myh10 in the epicardium : insights from the EHC mouse ». Thesis, University of Manchester, 2016. https://www.research.manchester.ac.uk/portal/en/theses/investigating-the-role-of-myh10-in-the-epicardium-insights-from-the-ehc-mouse(7d7cec65-e2e6-448c-a6d1-65d3fdc50f3e).html.

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Aim: Recent interest in cardiogenesis has focused on the epicardium, the outer epithelial layer that envelops the heart. Epicardial-derived cells (EPDCs) contribute vascular smooth muscle to developing coronary vessels and provide critical signalling cues to facilitate myocardial functionality. However, the precise molecular mechanisms that underpin epicardial biology remain unclear. Ablation of Myh10 in the EHC mouse results in embryonic lethal cardiac malformations, including epicardial and coronary defects. We sought to establish the role of Myh10 in epicardial cell function to further dissect the coronary vessel developmental pathway, a deeper understanding of which may inform the design of therapeutics to regenerate and repair the injured heart. Methods: Utilising multiple cell and developmental biology techniques, we generated a pathological evaluation of the EHC phenotype. EPDC migration was investigated in vivo with Wt1 immunohistochemistry, and in vitro by performing scratch wound assays on epicardial cell cultures. Congruently, we examined the ability of epicardial cells to undergo EMT in vivo by employing Snail and Phosphohistone-H3 immunohistochemistry. Results: Our studies reveal that EHC epicardial cells have a reduced capacity to invade the ventricular myocardium. Furthermore, we discovered increased proliferation and reduced Snail expression specifically within the EHC epicardium, consistent with EMT dysregulation. Interestingly, epicardial cell function did not appear to be disrupted in vitro. Conclusion: These results demonstrate a novel role for Myh10 in both EPDC migration and the promotion of epicardial EMT. Our finding that migration is unaffected in vitro suggests that the unique properties of the in vivo epicardial microenvironment dictate a requirement for Myh10 in order to elicit correct epicardial function. Together, this research enhances our understanding of the dysfunctional processes that contribute to abnormal cardiogenesis; these insights may aid our ability to determine the molecular regulators of coronary vessel development, and create therapeutics to regenerate vessel growth and repair injured cardiac tissue in cardiovascular disease.
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Livres sur le sujet "Cardiogenesi"

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Ltd, ICON Group. CARDIOGENESIS CORP. : Labor Productivity Benchmarks and International Gap Analysis (Labor Productivity Series). 2e éd. Icon Group International, 2000.

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Ltd, ICON Group. CARDIOGENESIS CORP. : International Competitive Benchmarks and Financial Gap Analysis (Financial Performance Series). 2e éd. Icon Group International, 2000.

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Chapitres de livres sur le sujet "Cardiogenesi"

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Kamp, Timothy J., et Gary E. Lyons. « Embryonic Stem Cells and Cardiogenesis ». Dans Cardiovascular Regeneration and Stem Cell Therapy, 25–35. Oxford, UK : Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988909.ch4.

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Turner, Nigel M., et Anneliese Nusmeier. « Cardiogene shock en hartfalen ». Dans APLS compact, 28–29. Houten : Bohn Stafleu van Loghum, 2019. http://dx.doi.org/10.1007/978-90-368-2221-3_24.

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Franco, Diego, Fernando Bonet, Francisco Hernandez-Torres, Estefania Lozano-Velasco, Francisco J. Esteban et Amelia E. Aranega. « Analysis of microRNA Microarrays in Cardiogenesis ». Dans Methods in Molecular Biology, 207–21. New York, NY : Springer New York, 2015. http://dx.doi.org/10.1007/7651_2015_247.

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Srivastava, Deepak. « Mechanisms of Cardiogenesis and Myocardial Development ». Dans Cardiovascular Development and Congenital Malformations, 25. Malden, Massachusetts, USA : Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.part2.

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Hatcher, Cathy J., Min-Su Kim, David Pennisi, Yan Song, Nata Diman, Marsha M. Goldstein, Takashi Mikawa et Craig T. Basson. « TBX5 Regulates Cardiac Cell Behavior During Cardiogenesis ». Dans Cardiovascular Development and Congenital Malformations, 27–30. Malden, Massachusetts, USA : Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.ch7.

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Wobus, A. M., J. Rohwedel, V. Maltsev et J. Hescheler. « Embryonic Stem Cell Derived Cardiogenesis and Myogenesis ». Dans Cell Culture in Pharmaceutical Research, 29–57. Berlin, Heidelberg : Springer Berlin Heidelberg, 1994. http://dx.doi.org/10.1007/978-3-662-03011-0_3.

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Kumar, Pavitra, Lakshmikirupa Sundaresan et Suvro Chatterjee. « Nitrosative Stress and Cardiogenesis : Cardiac Remodelling Perturbs Embryonic Metabolome ». Dans Modulation of Oxidative Stress in Heart Disease, 377–91. Singapore : Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-13-8946-7_15.

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Hatcher, Cathy J., et Craig T. Basson. « Holt-Oram Syndrome and the TBX5 Transcription Factor in Cardiogenesis ». Dans Molecular Genetics of Cardiac Electrophysiology, 297–315. Boston, MA : Springer US, 2000. http://dx.doi.org/10.1007/978-1-4615-4517-0_19.

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Ogura, Toshihiko. « Tbx5 Specifies the Left/Right Ventricles and Ventricular Septum Position During Cardiogenesis ». Dans Cardiovascular Development and Congenital Malformations, 75–77. Malden, Massachusetts, USA : Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.ch18.

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Hendrix, Anneke, Michiel L. Bots et Arend Mosterd. « Sudden Cardiac Death in the Young ; Epidemiology and Cardiogenetic Evaluation of Victims and Their Relatives ». Dans Clinical Cardiogenetics, 311–19. Cham : Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44203-7_19.

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Actes de conférences sur le sujet "Cardiogenesi"

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Wan, Chen-rei, Seok Chung, Ryo Sudo et Roger D. Kamm. « Induction of Cardiomyocyte Differentiation From Mouse Embryonic Stem Cells in a Confined Microfluidic Environment ». Dans ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-203995.

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Embryonic stem cell derived cardiomyocytes are deemed an attractive treatment option for myocardial infarction. Their clinical efficacy, however, has not been unequivocally demonstrated. There is a need for better understanding and characterization of the cardiogenesis process. A microfluidic platform in vitro is used to dissect and better understand the differentiation process. Through this study, we find that while embryoid bodies (EBs) flatten out in a well plate system, differentiated EBs self-assemble into complex 3D structures. The beating regions of EBs are also different. Most beating areas are observed in a ring pattern on 2D well plates around the center, self-assembled beating large 3D aggregates are found in microfluidic devices. Furthermore, inspired by the natural mechanical environment of the heart, we applied uniaxial cyclic mechanical stretch to EBs. Results suggest that prolonged mechanical stimulation acts as a negative regulator of cardiogenesis. From this study, we conclude that the culture environments can influence differentiation of embryonic stem cells into cardiomycytes, and that the use of microfluidic systems can provide new insights into the differentiation process.
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Sargent, Carolyn Y., Luke A. Hiatt, Sandhya Anantharaman, Eric Berson et Todd C. McDevitt. « Cardiogenesis of Embryonic Stem Cells is Modulated by Hydrodynamic Mixing Conditions ». Dans ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193129.

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Embryonic stem cells (ESCs) have the potential to differentiate into all somatic cell types and are uniquely capable of differentiating into functional cardiomyocytes; however, to effectively use ESCs for cell-based therapies to regenerate viable myocardial tissue, an improved understanding of mechanisms regulating differentiation is necessary. Currently, application of exogenous factors is commonly attempted to direct stem cell differentiation; however, progression towards controlling multiple environmental factors, including biochemical and mechanical stimuli, may result in increased differentiation efficiency for clinical applications. Additionally, current methods of ESC differentiation to cardiomyocytes are labor-intensive and produce relatively few cardiomyocytes based on initial ESC densities. Rotary suspension culture to produce embryoid bodies (EBs) has been shown to yield greater numbers of differentiating ESCs than static suspension cultures [1]. Thus, the objective of this study was to examine how the hydrodynamic mixing conditions imposed by rotary orbital culture modulate cardiomyocyte differentiation.
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Scully, Deirdre M., Andrew L. Lopez et Irina V. Larina. « Optogenetic investigation of mouse embryonic cardiogenesis with continuous-wave light stimulation ». Dans Diagnostic and Therapeutic Applications of Light in Cardiology 2022, sous la direction de Laura Marcu et Gijs van Soest. SPIE, 2022. http://dx.doi.org/10.1117/12.2609124.

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Lopez, Andrew L., Shang Wang et Irina V. Larina. « Live dynamic analysis of mouse embryonic cardiogenesis with functional optical coherence tomography ». Dans Diseases in the Breast and Reproductive System IV, sous la direction de Melissa C. Skala et Paul J. Campagnola. SPIE, 2018. http://dx.doi.org/10.1117/12.2292104.

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Larina, Irina V., Andrew L. Lopez et Shang Wang. « Functional optical coherence tomography for live dynamic analysis of mouse embryonic cardiogenesis ». Dans Dynamics and Fluctuations in Biomedical Photonics XV, sous la direction de Valery V. Tuchin, Kirill V. Larin, Martin J. Leahy et Ruikang K. Wang. SPIE, 2018. http://dx.doi.org/10.1117/12.2292106.

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Shabaldin, A. V., L. N. Igisheva et A. A. Rumyanceva. « CONTRIBUTION OF GENETIC PREDICTORS TO FORMATION OF HEALTH DEFICIENCY IN THE SEPARATE PERIOD AFTER CARDIAC SURGERY TREATMENT OF CONGENITAL HEART DEFECTS ». Dans I International Congress “The Latest Achievements of Medicine, Healthcare, and Health-Saving Technologies”. Kemerovo State University, 2023. http://dx.doi.org/10.21603/-i-ic-151.

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Objective: To study the contribution of xenobiotic biotransformation enzyme genes, transcription factors, inflammatory and immune response receptors in determining health deficiency in the separated period after cardiac surgery for congenital heart disease. Materials and methods. 116 children who underwent radical correction of CHD were examined. An assessment of the catamnesis of these children and genetic typing of genes encoding enzymes for the biotransformation of xeno- and endobiotics (GSTP, CYP1A2, CYP1A1), involved in the determination of cardiogenesis and processes in cardiomyocytes (CRELD-1, GATA-6, NOTCH-1), innate ( TREM-1) and adaptive (HLA-DR) immunity. The search for predictors of functioning deficit by physical, psycho-emotional, social, mental types was carried out using multiple logistic regression. Results. The level of functioning of various components of health one year after surgical treatment was associated with the same factors. These factors negatively affecting the health of children one year after heart surgery were: unfavorable living conditions, as well as genetic predictor markers HLA-DRB1*07 and Creld1 T/C (rs9878047)*T.
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