Relevant bibliographies by topics / Cardiogenesis

Academic literature on the topic 'Cardiogenesis'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "Cardiogenesis"

1

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

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2

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

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3

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

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4

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

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5

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

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

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

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8

Mukhopadhyay, Madhura. "Recapitulating early cardiogenesis in vitro." Nature Methods 18, no. 4 (April 2021): 331. http://dx.doi.org/10.1038/s41592-021-01118-2.

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9

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

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10

Fougerousse, Françoise, Louise V. B. Anderson, Anne-Lise Delezoide, Laurence Suel, Muriel Durand, and Jacques S. Beckmann. "Calpain3 expression during human cardiogenesis." Neuromuscular Disorders 10, no. 4-5 (June 2000): 251–56. http://dx.doi.org/10.1016/s0960-8966(99)00107-8.

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Dissertations / Theses on the topic "Cardiogenesis"

1

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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2

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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3

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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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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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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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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Akerberg, Alexander. "Contemporary Genetic Tools for in Vivo Investigations of H3K27 Demethylases in Zebrafish Cardiogenesis." Thesis, University of Oregon, 2016. http://hdl.handle.net/1794/20676.

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Dynamic histone modification has emerged as a robust and versatile regulator of gene expression in eukaryotic cells. One such modification, the trimethylation of lysine 27 on histone H3 (H3K27me3) is facilitated by the Polycomb repressive complex 2 (PRC2) and contributes to the localized repression of transcription. Subsequently, lysine specific demethylase Kdm6b (Jmjd3) can relieve the repressive H3K27me3 mark, allowing for transcriptional activation. In vitro studies have suggested a role for Kdm6b during mesodermal and cardiovascular differentiation in mammalian embryonic stem cells; however, this relationship has yet to be characterized in vivo. I utilized the advantages of the zebrafish model to investigate the in vivo roles of Kdm6b-family demethylases during development using a reverse genetic approach. I carried out two independent loss-of-function studies to analyze the role of Kdm6b-family demethylases during embryonic development in zebrafish. By comparing genetic loss-of-function and morpholino-mediated knockdown approaches, I found that morpholino–mediated knockdown of kdm6bb transcript produces off-target effects and does not portray an accurate representation of in vivo function. I then show that, while not required for early cardiogenesis, histone demethylases kdm6ba and kdm6bb function redundantly to promote late stage proliferation during heart ventricle trabeculation. These data reveal a previously unknown functional relationship and support the hypothesis that Kdm6b-family demethylases function primarily during later stages of development. Additionally, my description of morpholino-induced off-target effects supports the need to use extreme caution when interpreting morphant phenotypes. Due to the embryonic lethality exhibited by kdm6b-deficient embryos and the limited tools available for spatiotemporal transgene control in zebrafish, I was unable to investigate demethylase function within adult animals. I attempted to circumvent these limitations by creating an inducible gene expression system that uses tissue-specific transgenes that express the Gal4 transcription factor fused to the estrogen-binding domain of the human estrogen receptor. I showed that these Gal4-ERT driver lines confer rapid, tissue-specific induction of UAS-controlled transgenes following tamoxifen exposure in both embryos and adult fish. I then demonstrated how this technology could be used to define developmental windows of gene function by spatiotemporally controlling expression of constitutively active Notch1 in embryos. This dissertation contains previously published co-authored material.
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9

Kaarbo, Mari, and n/a. "The Role of RhoA in Early Heart Development." Griffith University. School of Biomolecular and Biomedical Science, 2005. http://www4.gu.edu.au:8080/adt-root/public/adt-QGU20060105.091005.

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RhoA is a small GTPase that acts as a molecular switch to control a variety of signal transduction pathways in eukaryotes. From an initial established role in the regulation of the actin cytoskeleton, RhoA has now been implicated in a range of functions that include gene transcription and regulation of cell morphology. In earlier studies from this laboratory that employed differential display and in situ hybridisation, RhoA was indicated as being up-regulated during the stages of early heart development in the developing chick embryo. Given the important effects of RhoA on both gene expression and morphology in other systems, it was hypothesised that RhoA plays a central role in the molecular mechanisms controlling cardiogenesis. This thesis describes investigations undertaken to elucidate the role of RhoA in these processes. As an initial approach to corroborate the earlier gene expression findings and provide further evidence for a role in tissue developmental mechanisms, RhoA proteins levels in the developing chick embryo were analysed using immunocytochemistry. These experiments demonstrated that RhoA is most abundant in heart-forming regions, findings compatible with the earlier gene expression studies and the proposed role of this protein in early heart development. Preliminary studies from this laboratory had also suggested that chick RhoA is expressed as different length mRNA transcripts that vary only in the 3' untranslated region (UTR). This thesis presents additional evidence for the existence of these different RhoA transcripts from experiments using Northern hybridisation and RT-PCR analyses. These analyses also serve to demonstrate that the second shortest RhoA transcript (designated RhoA2) is the most abundant transcript in developing heart tissue, in contrast to the situation in other embryonic tissues, findings that could be taken to suggest a possible role for this 3'UTR in developmental mechanisms that is yet to be elucidated. One potentially informative approach for testing the function of a protein in a biological system is to inhibit its expression and/or activity and observe the changes induced. The effects of inhibiting RhoA in early heart development and early organogenesis in the chick embryo model were investigated using small interfering RNAs (siRNA). Reduction in RhoA expression by siRNA treatment, as confirmed by real-time PCR, resulted in loss of heart tube fusion and abnormal head development, the former result providing further direct evidence of a role for RhoA in heart developmental processes. In order to investigate the function of RhoA specifically during the process of cardiomyocyte differentiation, an inducible model of cardiomyogenesis, P19CL6 cells, was used in combination with over-expression of different forms of mouse RhoA. The striking result from these investigations was that over-expression of the dominant negative mutant of mouse RhoA (mRhoAN19) prevented the differentiation of induced P19CL6 cells to the cardiomyocyte phenotype, results consistent with an essential role for RhoA in this cellular transition. The mechanism by which RhoA mediates its different cellular functions is unclear, however some studies have implicated RhoA in the regulation of transcription factors. To investigate such a mechanism as a possible explanation for the requirement of RhoA in cardiomyocyte differentiation, the P19CL6 inducible cell system over-expressing different forms of RhoA was analysed through real-time PCR to quantify the levels of transcription of genes known to play an important role in early heart development. These investigations indicated that RhoA inhibition causes an accumulation of the cardiac transcription factors SRF and GATA4 and the early cardiac marker cardiac-cx-actin. The expression of a protein is controlled by, among other factors, regulatory proteins that control transcription. To investigate factors in heart that potentially regulate RhoA expression at the molecular level, the chick RhoA gene organisation was analysed. The gene was shown to contain three introns that interrupt the protein coding sequence and at least one intron in the 5'UTR. Comparative RhoA gene studies indicated both an almost identical organisation and coding sequence of the chick, mouse and human RhoA genes, indicative of strict conservation of this gene during evolution. The putative promoter region of RhoA was predicted by computer analyses and tested for promoter activity using luciferase reporter analyses in non-differentiated and differentiated cardiomyocytes, using the inducible P19CL6 cell system. These investigations served to define a putative core promoter region that exhibited significantly higher promoter activity in differentiated cardiomyocytes than in non-differentiated cells, and other elements upstream of this core region that appear to be required for transcriptional regulation of RhoA. The majority of the consensus transcription factor sites identified in this putative promoter have been previously implicated in either heart development and/or organogenesis. These results therefore provide further, although indirect, evidence for an important role for RhoA in the molecular mechanisms controlling both cardiogenesis and embryogenesis in general. In summary, this thesis provides novel information on the role of RhoA in the processes of cardiogenesis and provides a firm foundation for continuing investigations aimed at elucidating the molecular basis of this contribution.
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Kaarbo, Mari. "The Role of RhoA in Early Heart Development." Thesis, Griffith University, 2005. http://hdl.handle.net/10072/366791.

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RhoA is a small GTPase that acts as a molecular switch to control a variety of signal transduction pathways in eukaryotes. From an initial established role in the regulation of the actin cytoskeleton, RhoA has now been implicated in a range of functions that include gene transcription and regulation of cell morphology. In earlier studies from this laboratory that employed differential display and in situ hybridisation, RhoA was indicated as being up-regulated during the stages of early heart development in the developing chick embryo. Given the important effects of RhoA on both gene expression and morphology in other systems, it was hypothesised that RhoA plays a central role in the molecular mechanisms controlling cardiogenesis. This thesis describes investigations undertaken to elucidate the role of RhoA in these processes. As an initial approach to corroborate the earlier gene expression findings and provide further evidence for a role in tissue developmental mechanisms, RhoA proteins levels in the developing chick embryo were analysed using immunocytochemistry. These experiments demonstrated that RhoA is most abundant in heart-forming regions, findings compatible with the earlier gene expression studies and the proposed role of this protein in early heart development. Preliminary studies from this laboratory had also suggested that chick RhoA is expressed as different length mRNA transcripts that vary only in the 3' untranslated region (UTR). This thesis presents additional evidence for the existence of these different RhoA transcripts from experiments using Northern hybridisation and RT-PCR analyses. These analyses also serve to demonstrate that the second shortest RhoA transcript (designated RhoA2) is the most abundant transcript in developing heart tissue, in contrast to the situation in other embryonic tissues, findings that could be taken to suggest a possible role for this 3'UTR in developmental mechanisms that is yet to be elucidated. One potentially informative approach for testing the function of a protein in a biological system is to inhibit its expression and/or activity and observe the changes induced. The effects of inhibiting RhoA in early heart development and early organogenesis in the chick embryo model were investigated using small interfering RNAs (siRNA). Reduction in RhoA expression by siRNA treatment, as confirmed by real-time PCR, resulted in loss of heart tube fusion and abnormal head development, the former result providing further direct evidence of a role for RhoA in heart developmental processes. In order to investigate the function of RhoA specifically during the process of cardiomyocyte differentiation, an inducible model of cardiomyogenesis, P19CL6 cells, was used in combination with over-expression of different forms of mouse RhoA. The striking result from these investigations was that over-expression of the dominant negative mutant of mouse RhoA (mRhoAN19) prevented the differentiation of induced P19CL6 cells to the cardiomyocyte phenotype, results consistent with an essential role for RhoA in this cellular transition. The mechanism by which RhoA mediates its different cellular functions is unclear, however some studies have implicated RhoA in the regulation of transcription factors. To investigate such a mechanism as a possible explanation for the requirement of RhoA in cardiomyocyte differentiation, the P19CL6 inducible cell system over-expressing different forms of RhoA was analysed through real-time PCR to quantify the levels of transcription of genes known to play an important role in early heart development. These investigations indicated that RhoA inhibition causes an accumulation of the cardiac transcription factors SRF and GATA4 and the early cardiac marker cardiac-cx-actin. The expression of a protein is controlled by, among other factors, regulatory proteins that control transcription. To investigate factors in heart that potentially regulate RhoA expression at the molecular level, the chick RhoA gene organisation was analysed. The gene was shown to contain three introns that interrupt the protein coding sequence and at least one intron in the 5'UTR. Comparative RhoA gene studies indicated both an almost identical organisation and coding sequence of the chick, mouse and human RhoA genes, indicative of strict conservation of this gene during evolution. The putative promoter region of RhoA was predicted by computer analyses and tested for promoter activity using luciferase reporter analyses in non-differentiated and differentiated cardiomyocytes, using the inducible P19CL6 cell system. These investigations served to define a putative core promoter region that exhibited significantly higher promoter activity in differentiated cardiomyocytes than in non-differentiated cells, and other elements upstream of this core region that appear to be required for transcriptional regulation of RhoA. The majority of the consensus transcription factor sites identified in this putative promoter have been previously implicated in either heart development and/or organogenesis. These results therefore provide further, although indirect, evidence for an important role for RhoA in the molecular mechanisms controlling both cardiogenesis and embryogenesis in general. In summary, this thesis provides novel information on the role of RhoA in the processes of cardiogenesis and provides a firm foundation for continuing investigations aimed at elucidating the molecular basis of this contribution.
Thesis (PhD Doctorate)
Doctor of Philosophy (PhD)
School of Biomolecular and Biomedical Sciences
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Books on the topic "Cardiogenesis"

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Baars, H. F., P. A. F. M. Doevendans, and J. J. van der Smagt, eds. Clinical Cardiogenetics. London: Springer London, 2011. http://dx.doi.org/10.1007/978-1-84996-471-5.

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Baars, Hubert F., Pieter A. F. M. Doevendans, Arjan C. Houweling, and J. Peter van Tintelen, eds. Clinical Cardiogenetics. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44203-7.

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Baars, Hubert F., Pieter A. F. M. Doevendans, Arjan C. Houweling, and J. Peter van Tintelen, eds. Clinical Cardiogenetics. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-45457-9.

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Baars, H. F. Clinical Cardiogenetics. London: Springer-Verlag London Limited, 2011.

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

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

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Baars, Hubert F., Pieter A. F. M. Doevendans, Arjan C. Houweling, and J. Peter van Tintelen. Clinical Cardiogenetics. Springer, 2016.

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Baars, Hubert F., Pieter A. F. M. Doevendans, Arjan C. Houweling, and J. Peter van Tintelen. Clinical Cardiogenetics. Springer, 2016.

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Baars, Hubert F., Pieter A. F. M. Doevendans, Arjan C. Houweling, and J. Peter van Tintelen. Clinical Cardiogenetics. Springer International Publishing AG, 2021.

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Baars, Hubert F., Pieter A. F. M. Doevendans, Arjan C. Houweling, and J. Peter van Tintelen. Clinical Cardiogenetics. Springer, 2020.

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Book chapters on the topic "Cardiogenesis"

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Kamp, Timothy J., and Gary E. Lyons. "Embryonic Stem Cells and Cardiogenesis." In 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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Franco, Diego, Fernando Bonet, Francisco Hernandez-Torres, Estefania Lozano-Velasco, Francisco J. Esteban, and Amelia E. Aranega. "Analysis of microRNA Microarrays in Cardiogenesis." In 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." In 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, and Craig T. Basson. "TBX5 Regulates Cardiac Cell Behavior During Cardiogenesis." In 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, and J. Hescheler. "Embryonic Stem Cell Derived Cardiogenesis and Myogenesis." In 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, and Suvro Chatterjee. "Nitrosative Stress and Cardiogenesis: Cardiac Remodelling Perturbs Embryonic Metabolome." In 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., and Craig T. Basson. "Holt-Oram Syndrome and the TBX5 Transcription Factor in Cardiogenesis." In 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." In 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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Cornel, Martina C., Isa Houwink, and Christopher Semsarian. "Future of Cardiogenetics." In Clinical Cardiogenetics, 389–93. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-44203-7_24.

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Zafarmand, Mohammad Hadi, K. David Becker, and Pieter A. Doevendans. "Future of Cardiogenetics." In Clinical Cardiogenetics, 437–42. London: Springer London, 2010. http://dx.doi.org/10.1007/978-1-84996-471-5_28.

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Conference papers on the topic "Cardiogenesis"

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Wan, Chen-rei, Seok Chung, Ryo Sudo, and Roger D. Kamm. "Induction of Cardiomyocyte Differentiation From Mouse Embryonic Stem Cells in a Confined Microfluidic Environment." In 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, and Todd C. McDevitt. "Cardiogenesis of Embryonic Stem Cells is Modulated by Hydrodynamic Mixing Conditions." In 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, and Irina V. Larina. "Optogenetic investigation of mouse embryonic cardiogenesis with continuous-wave light stimulation." In Diagnostic and Therapeutic Applications of Light in Cardiology 2022, edited by Laura Marcu and Gijs van Soest. SPIE, 2022. http://dx.doi.org/10.1117/12.2609124.

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Lopez, Andrew L., Shang Wang, and Irina V. Larina. "Live dynamic analysis of mouse embryonic cardiogenesis with functional optical coherence tomography." In Diseases in the Breast and Reproductive System IV, edited by Melissa C. Skala and Paul J. Campagnola. SPIE, 2018. http://dx.doi.org/10.1117/12.2292104.

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

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Shabaldin, A. V., L. N. Igisheva, and A. A. Rumyanceva. "CONTRIBUTION OF GENETIC PREDICTORS TO FORMATION OF HEALTH DEFICIENCY IN THE SEPARATE PERIOD AFTER CARDIAC SURGERY TREATMENT OF CONGENITAL HEART DEFECTS." In 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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