Gotowe bibliografie tematyczne / Cardiomyogenesis

Gotowa bibliografia na temat „Cardiomyogenesis”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 19 lutego 2023

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Artykuły w czasopismach na temat "Cardiomyogenesis"

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Gomez, José A., Alan Payne, Richard E. Pratt, Conrad P. Hodgkinson i Victor J. Dzau. "A role for Sfrp2 in cardiomyogenesis in vivo". Proceedings of the National Academy of Sciences 118, nr 33 (11.08.2021): e2103676118. http://dx.doi.org/10.1073/pnas.2103676118.

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Cardiomyogenesis, the process by which the body generates cardiomyocytes, is poorly understood. We have recently shown that Sfrp2 promotes cardiomyogenesis in vitro. The objective of this study was to determine if Sfrp2 would similarly promote cardiomyogenesis in vivo. To test this hypothesis, we tracked multipotent cKit(+) cells in response to Sfrp2 treatment. In control adult mice, multipotent cKit(+) cells typically differentiated into endothelial cells but not cardiomyocytes. In contrast, Sfrp2 switched the fate of these cells. Following Sfrp2 injection, multipotent cKit(+) cells differentiated solely into cardiomyocytes. Sfrp2-derived cardiomyocytes integrated into the myocardium and exhibited identical physiological properties to preexisting native cardiomyocytes. The ability of Sfrp2 to promote cardiomyogenesis was further supported by tracking EdU-labeled cells. In addition, Sfrp2 did not promote the formation of new cardiomyocytes when the cKit(+) cell population was selectively ablated in vivo using a diphtheria toxin receptor–diphtheria toxin model. Notably, Sfrp2-induced cardiomyogenesis was associated with significant functional improvements in a cardiac injury model. In summary, our study further demonstrates the importance of Sfrp2 in cardiomyogenesis.
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Li, Haobo, Lena E. Trager, Xiaojun Liu, Margaret H. Hastings, Chunyang Xiao, Justin Guerra, Samantha To i in. "lncExACT1 and DCHS2 Regulate Physiological and Pathological Cardiac Growth". Circulation 145, nr 16 (19.04.2022): 1218–33. http://dx.doi.org/10.1161/circulationaha.121.056850.

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Background: The heart grows in response to pathological and physiological stimuli. The former often precedes cardiomyocyte loss and heart failure; the latter paradoxically protects the heart and enhances cardiomyogenesis. The mechanisms underlying these differences remain incompletely understood. Although long noncoding RNAs (lncRNAs) are important in cardiac development and disease, less is known about their roles in physiological hypertrophy or cardiomyogenesis. Methods: RNA sequencing was applied to hearts from mice after 8 weeks of voluntary exercise-induced physiological hypertrophy and cardiomyogenesis or transverse aortic constriction for 2 or 8 weeks to induce pathological hypertrophy or heart failure. The top lncRNA candidate was overexpressed in hearts with adeno-associated virus vectors and inhibited with antisense locked nucleic acid–GapmeRs to examine its function. Downstream effectors were identified through promoter analyses and binding assays. The functional roles of a novel downstream effector, dachsous cadherin-related 2 (DCHS2), were examined through transgenic overexpression in zebrafish and cardiac-specific deletion in Cas9-knockin mice. Results: We identified exercise-regulated cardiac lncRNAs, called lncExACTs. lncExACT1 was evolutionarily conserved and decreased in exercised hearts but increased in human and experimental heart failure. Cardiac lncExACT1 overexpression caused pathological hypertrophy and heart failure; lncExACT1 inhibition induced physiological hypertrophy and cardiomyogenesis, protecting against cardiac fibrosis and dysfunction. lncExACT1 functioned by regulating microRNA-222, calcineurin signaling, and Hippo/Yap1 signaling through DCHS2. Cardiomyocyte DCHS2 overexpression in zebrafish induced pathological hypertrophy and impaired cardiac regeneration, promoting scarring after injury. In contrast, murine DCHS2 deletion induced physiological hypertrophy and promoted cardiomyogenesis. Conclusions: These studies identify lncExACT1-DCHS2 as a novel pathway regulating cardiac hypertrophy and cardiomyogenesis. lncExACT1-DCHS2 acts as a master switch toggling the heart between physiological and pathological growth to determine functional outcomes, providing a potentially tractable therapeutic target for harnessing the beneficial effects of exercise.
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Sepac, Ana, Zeljko J. Bosnjak, Sven Seiwerth, Suncana Sikiric, Tihana Regovic Dzombeta, Ana Kulic, Jelena Marunica Karsaj i Filip Sedlic. "Human C2a and C6a iPSC lines and H9 ESC line have less efficient cardiomyogenesis than H1 ESC line: Beating enhances cardiac differentiation". International Journal of Developmental Biology 65, nr 10-11-12 (2021): 537–43. http://dx.doi.org/10.1387/ijdb.210115fs.

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Background: Human induced pluripotent stem cells (hiPSCs) need to be thoroughly characterized to exploit their potential advantages in various aspects of biomedicine. The aim of this study was to compare the efficiency of cardiomyogenesis of two hiPSCs and two human embryonic stem cell (hESC) lines by genetic living cardiomyocyte labeling. We also analyzed the influence of spontaneous beating on cardiac differentiation. Methods: H1 and H9 hESC lines and C2a and C6a hiPSC lines were induced into in vitro directed cardiac differentiation. Cardiomyogenesis was evaluated by the analysis of cell cluster beating, cardiac protein expression by immunocytochemistry, ability of cells to generate calcium transients, and cardiomyocyte quantification by the myosin light chain 2v-enhanced green fluorescent protein gene construct delivered with a lentiviral vector. Results: Differentiation of all cell lines yielded spontaneously beating cell clusters, indicating the presence of functional cardiomyocytes. After the cell dissociation, H1-hESC-derived cardiomyocytes exhibited spontaneous calcium transients, corresponding to autonomous electrical activity and displayed ability to transmit them between the cells. Differentiated hESC and hiPSC cells exhibited striated sarcomeres and expressed cardiac proteins sarcomeric α-actinin and cardiac troponin T. Cardiomyocytes were the most abundant in differentiated H1 hESC line (20% more than in other tested lines). In all stem cell lines, cardiomyocyte enrichment was greater in beating than in non-beating cell clusters, irrespective of cardiomyogenesis efficiency. Conclusion: Although C2a and C6a hiPSC and H9 hESC lines exhibited efficient cardiomyogenesis, H1 hESC line yielded the greatest cardiomyocyte enrichment of all tested lines. Beating of cell clusters promotes cardiomyogenesis in tested hESCs and hiPSCs.
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Lerchenmüller, Carolin, Ana Vujic, Sonja Mittag, Annie Wang, Charles P. Rabolli, Chiara Heß, Fynn Betge i in. "Restoration of Cardiomyogenesis in Aged Mouse Hearts by Voluntary Exercise". Circulation 146, nr 5 (2.08.2022): 412–26. http://dx.doi.org/10.1161/circulationaha.121.057276.

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Background: The human heart has limited capacity to generate new cardiomyocytes and this capacity declines with age. Because loss of cardiomyocytes may contribute to heart failure, it is crucial to explore stimuli of endogenous cardiac regeneration to favorably shift the balance between loss of cardiomyocytes and the birth of new cardiomyocytes in the aged heart. We have previously shown that cardiomyogenesis can be activated by exercise in the young adult mouse heart. Whether exercise also induces cardiomyogenesis in aged hearts, however, is still unknown. Here, we aim to investigate the effect of exercise on the generation of new cardiomyocytes in the aged heart. Methods: Aged (20-month-old) mice were subjected to an 8-week voluntary running protocol, and age-matched sedentary animals served as controls. Cardiomyogenesis in aged hearts was assessed on the basis of 15 N-thymidine incorporation and multi-isotope imaging mass spectrometry. We analyzed 1793 cardiomyocytes from 5 aged sedentary mice and compared these with 2002 cardiomyocytes from 5 aged exercised mice, followed by advanced histology and imaging to account for ploidy and nucleation status of the cell. RNA sequencing and subsequent bioinformatic analyses were performed to investigate transcriptional changes induced by exercise specifically in aged hearts in comparison with young hearts. Results: Cardiomyogenesis was observed at a significantly higher frequency in exercised compared with sedentary aged hearts on the basis of the detection of mononucleated/diploid 15 N-thymidine–labeled cardiomyocytes. No mononucleated/diploid 15 N-thymidine–labeled cardiomyocyte was detected in sedentary aged mice. The annual rate of mononucleated/diploid 15 N-thymidine–labeled cardiomyocytes in aged exercised mice was 2.3% per year. This compares with our previously reported annual rate of 7.5% in young exercised mice and 1.63% in young sedentary mice. Transcriptional profiling of young and aged exercised murine hearts and their sedentary controls revealed that exercise induces pathways related to circadian rhythm, irrespective of age. One known oscillating transcript, however, that was exclusively upregulated in aged exercised hearts, was isoform 1.4 of regulator of calcineurin, whose regulation and functional role were explored further. Conclusions: Our data demonstrate that voluntary running in part restores cardiomyogenesis in aged mice and suggest that pathways associated with circadian rhythm may play a role in physiologically stimulated cardiomyogenesis.
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Yasuda, Satoshi, Tetsuya Hasegawa, Tetsuji Hosono, Mitsutoshi Satoh, Kei Watanabe, Kageyoshi Ono, Shunichi Shimizu i in. "AW551984: a novel regulator of cardiomyogenesis in pluripotent embryonic cells". Biochemical Journal 437, nr 2 (28.06.2011): 345–55. http://dx.doi.org/10.1042/bj20110520.

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An understanding of the mechanism that regulates the cardiac differentiation of pluripotent stem cells is necessary for the effective generation and expansion of cardiomyocytes as cell therapy products. In the present study, we have identified genes that modulate the cardiac differentiation of pluripotent embryonic cells. We isolated P19CL6 cell sublines that possess distinct properties in cardiomyogenesis and extracted 24 CMR (cardiomyogenesis-related candidate) genes correlated with cardiomyogenesis using a transcriptome analysis. Knockdown of the CMR genes by RNAi (RNA interference) revealed that 18 genes influence spontaneous contraction or transcript levels of cardiac marker genes in EC (embryonal carcinoma) cells. We also performed knockdown of the CMR genes in mouse ES (embryonic stem) cells and induced in vitro cardiac differentiation. Three CMR genes, AW551984, 2810405K02Rik (RIKEN cDNA 2810405K02 gene) and Cd302 (CD302 antigen), modulated the cardiac differentiation of both EC cells and ES cells. Depletion of AW551984 attenuated the expression of the early cardiac transcription factor Nkx2.5 (NK2 transcription factor related locus 5) without affecting transcript levels of pluripotency and early mesoderm marker genes during ES cell differentiation. Activation of Wnt/β-catenin signalling enhanced the expression of both AW551984 and Nkx2.5 in ES cells during embryoid body formation. Our findings indicate that AW551984 is a novel regulator of cardiomyogenesis from pluripotent embryonic cells, which links Wnt/β-catenin signalling to Nkx2.5 expression.
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Kajstura, Jan, Konrad Urbanek, Shira Perl, Toru Hosoda, Hanqiao Zheng, Barbara Ogórek, João Ferreira-Martins i in. "Cardiomyogenesis in the Adult Human Heart". Circulation Research 107, nr 2 (23.07.2010): 305–15. http://dx.doi.org/10.1161/circresaha.110.223024.

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Habib, Manhal, Oren Caspi i Lior Gepstein. "Human embryonic stem cells for cardiomyogenesis". Journal of Molecular and Cellular Cardiology 45, nr 4 (październik 2008): 462–74. http://dx.doi.org/10.1016/j.yjmcc.2008.08.008.

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Ali, Enas Hussein, Fatemeh Sharifpanah, Amer Taha, Suk Ying Tsang, Maria Wartenberg i Heinrich Sauer. "The Milk Thistle (Silybum marianum) Compound Silibinin Inhibits Cardiomyogenesis of Embryonic Stem Cells by Interfering with Angiotensin II Signaling". Stem Cells International 2018 (13.12.2018): 1–10. http://dx.doi.org/10.1155/2018/9215792.

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The milk thistle (Silybum marianum (L.) Gaertn.) compound silibinin may be an inhibitor of the angiotensin II type 1 (AT1) receptor which is expressed in differentiating embryonic stem (ES) cells and is involved in the regulation of cardiomyogenesis. In the present study, it was demonstrated that silibinin treatment decreased the number of spontaneously contracting cardiac foci and cardiac cell areas differentiated from ES cells as well as contraction frequency and frequency of calcium (Ca2+) spiking. In contrast, angiotensin II (Ang II) treatment stimulated cardiomyogenesis as well as contraction and Ca2+ spiking frequency, which were abolished in the presence of silibinin. Intracellular Ca2+ transients elicited by Ang II in rat smooth muscle cells were not impaired upon silibinin treatment, excluding the possibility that the compound acted on the AT1 receptor. Ang II treatment activated extracellular signal-regulated kinase 1/2 (ERK1/2), c-Jun NH2-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) pathways in embryoid bodies which were abolished upon silibinin pretreatment. In summary, our data suggest that silibinin inhibits cardiomyogenesis of ES cells by interfering with Ang II signaling downstream of the AT1 receptor.
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Humpolíček, P., K. A. Radaszkiewicz, V. Kašpárková, J. Stejskal, M. Trchová, Z. Kuceková, H. Vičarová, J. Pacherník, M. Lehocký i A. Minařík. "Stem cell differentiation on conducting polyaniline". RSC Advances 5, nr 84 (2015): 68796–805. http://dx.doi.org/10.1039/c5ra12218j.

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Mobley, Stephen, Jessica M. Shookhof, Kara Foshay, Michelle Park i G. Ian Gallicano. "PKG and PKC Are Down-Regulated during Cardiomyocyte Differentiation from Embryonic Stem Cells: Manipulation of These Pathways Enhances Cardiomyocyte Production". Stem Cells International 2010 (2010): 1–10. http://dx.doi.org/10.4061/2010/701212.

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Understanding signal transduction mechanisms that drive differentiation of adult or embryonic stem cells (ESCs) is imperative if they are to be used to cure disease. While the list of signaling pathways regulating stem cell differentiation is growing, it is far from complete. Indentifying regulatory mechanisms and timecourse commitment to cell lineages is needed for generating pure populations terminally differentiated cell types, and in ESCs, suppression of teratoma formation. To this end, we investigated specific signaling mechanisms involved in cardiomyogenesis, followed by manipulation of these pathways to enhance differentiation of ESCs into cardiomyocytes. Subjecting nascent ESC-derived cardiomyocytes to a proteomics assay, we found that cardiomyogenesis is influenced by up- and down-regulation of a number of kinases, one of which, cGMP-dependent protein kinase (PKG), is markedly down-regulated during differentiation. Delving further, we found that manipulating the PKG pathway using PKG-specific inhibitors produced significantly more cardiomyocytes from ESCs when compared to ESCs left to differentiate without inhibitors. In addition, we found combinatorial effects when culturing ESCs in inhibitors to PKG and PKC isotypes. Consequently, we have generated a novel hypothesis: Down-regulation of PKG and specific PKC pathways are necessary for cardiomyogenesis, and when manipulated, these pathways produce significantly more cardiomyocytes than untreated ESCs.
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Rozprawy doktorskie na temat "Cardiomyogenesis"

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Horton, Renita Elillian. "The Role of Microenvironmental Cues in Cardiomyogenesis and Pathogenesis". Thesis, Harvard University, 2014. http://dissertations.umi.com/gsas.harvard:11569.

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The cellular microenvironment consists of soluble and insoluble factors that provide signals that dictate cell behavior and cell fate. Limited characterization has hindered our ability to mimic the physiological or pathophysiological environment. While stem cells have vast promise in the areas of regenerative medicine and disease therapy, harnessing this potential remains elusive due to our limited understanding of differentiation mechanisms. Similarly, many in vitro cardiac disease models lack the critical structure- function relationships of healthy and diseased cardiac tissue. The goal of this work is to induce cardiomyogenesis and pathogenesis in vitro by recapitulating features of the native microenvironment during development and disease.
Engineering and Applied Sciences
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Teo, Ailing. "Exploring new bioprocess considerations for cardiomyogenesis of embryonic stem cells". Thesis, Imperial College London, 2013. http://hdl.handle.net/10044/1/24460.

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Ex vivo cardiomyocytes production from pluripotent stem cells is highly attractive as a future clinical therapy for cardiovascular diseases. Scaled-up 3-dimensional cell culture can be used to produce clinically relevant cell numbers but requires numerous bioprocess design considerations. In this thesis, we employed hydrogel encapsulation of mouse embryonic stem cells (mESCs) to study various novel design parameters that could be used for large-scale cardiomyocyte production. First, we demonstrated that our novel rotary, perfused bioreactor provided a dynamic and perfused environment that was superior to a commercial rotary wall bioreactor and conventional tissue culture vessels in terms of cell numbers and cardiac differentiation. With this novel bioreactor, we had also investigated the effects of pH on cardiomyogenesis. Cardiomyogenesis was found to be sensitive to different pH values, where slight fluctuations could cause significant changes to cell proliferation and cardiac differentiation. Last but not least, we utilised ultrasound as a novel mechanical stimulus for cardiac differentiation of mESCs and demonstrated its benefits in improving cardiomyocyte yield.
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Bosiljcic, Neven. "Enhancing Cardiomyogenesis In Stem Cells With the Use of Small Molecules". Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34304.

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Cardiovascular diseases contribute a large amount of morbidity and mortality in developing and developed countries all around the world. In conditions such as the myocardial infarction, a significant amount of cardiomyocytes die leading to an impaired function of the heart. One promising method for replacing these cardiomyocytes would be with the use of cardiomyocytes derived from embryonic stem cells. However, a large number of cardiomyocytes and a highly efficient method for obtaining cardiomyocytes are needed. Using the principles of small molecule treatment to induce differentiation in a serum-free based differentiation protocol, I have demonstrated that the induction of canonical Wnt signalling via CHIR 99021, and subsequent addition of bone morphogenetic protein 4 was best able to induce cardiomyogenesis in mouse embryonic stem cells. While improvements in efficiency are still required, the manipulation of the Wnt and BMP4 signalling pathways hold great promise in improving cardiomyogenesis in mESCs.
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Yilbas, Ayse Elif. "Molecular Basis of GATA-4 Expression During the Early Commitment Stage of Cardiomyogenesis". Thesis, Université d'Ottawa / University of Ottawa, 2015. http://hdl.handle.net/10393/31993.

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Cardiovascular diseases are among the leading causes of death in North America. Currently, there are no effective treatment options for directly repairing the damaged myocardial tissue. Therefore, cell-based therapies utilizing cardiomyocytes generated from stem cells to replace necrotic tissue will be a promising approach. However, the molecular mechanisms regulating stem cell differentiation into cardiomyocytes are not fully understood. Since GATA-4 is one of the primary regulators of cradiomyogenesis, we investigated the molecular basis of GATA-4 expression during the early stages of stem cell differentiation. Using chromatin immunoprecipitation, we have observed the direct involvement of p300 in GATA-4 gene expression. We have also examined the importance ofhHistone acetylation and acetyltransferase activity on GATA-4 expression during the early stage of cardiomyogensis using the histone deactylase inhibitor Valproic Acid and the acetyltransferase inhibitor Curcumin respectively.
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Pelaez, Daniel. "Role of Mechanical Strain on the Cardiomyogenic Differentiation of Periodontal Ligament Derived Stem Cells". Scholarly Repository, 2011. http://scholarlyrepository.miami.edu/oa_dissertations/573.

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The application of cellular therapies for the treatment of myocardial infarction has provided encouraging evidence for the possibility of cellular therapies to restore normal heart function. However, questions still remain as to the optimal cell source, pre-conditioning methods and delivery techniques for such an application. Here I propose the use of a unique population of stem cells arising from the embryonic neural crest. These cells were shown to express neural crest markers as well as pluripotency-associated markers. Furthermore, the cells were shown to express proteins essential to the formation of gap junctions and to possess a cardiomyogenic differentiation potential by several means. Furthermore, I explore the use of mechanical strain as an inducer of cardiomyogenesis and possibly pre-conditioning stimulus for the better engraftment of the cells while in the heart. Mechanical strain was shown to elicit a cardiomyogenic response from the cells following just a couple of hours of stimulation. The mode in which mechanical strain elicited these responses was demonstrated to be via the mediation of the reactive oxygen species (ROS) pathways. Given the results presented here, the use of these periodontal ligament-derived stem cells (PDLSC) in combination with mechanical strain preconditioning of the cells prior to their delivery into the heart may pose a valuable alternative for the treatment of myocardial infarction and merits further exploration for its capacity to augment the already observed beneficial effects of cellular therapies.
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Kaarbo, Mari, i 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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Wang, Qin. "Aryl Hydrocarbon Receptor-Mediated Regulation of Gene Expression during Cardiomyocyte Differentiation". University of Cincinnati / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1439307738.

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Voronova, Anastassia. "The Transcriptional Regulation of Stem Cell Differentiation Programs by Hedgehog Signalling". Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23223.

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The Hedgehog (Hh) signalling pathway is one of the key signalling pathways orchestrating intricate organogenesis, including the development of neural tube, heart and skeletal muscle. Yet, insufficient mechanistic understanding of its diverse roles is available. Here, we show the molecular mechanisms regulating the neurogenic, cardiogenic and myogenic properties of Hh signalling, via effector protein Gli2, in embryonic and adult stem cells. In Chapter 2, we show that Gli2 induces neurogenesis, whereas a dominant-negative form of Gli2 delays neurogenesis in P19 embryonal carcinoma (EC) cells, a mouse embryonic stem (ES) cell model. Furthermore, we demonstrate that Gli2 associates with Ascl1/Mash1 gene elements in differentiating P19 cells and activates the Ascl1/Mash1 promoter in vitro. Thus, Gli2 mediates neurogenesis in P19 cells at least in part by directly regulating Ascl1/Mash1 expression. In Chapter 3, we demonstrate that Gli2 and MEF2C bind each other’s regulatory elements and regulate each other’s expression while enhancing cardiomyogenesis in P19 cells. Furthermore, dominant-negative Gli2 and MEF2C proteins downregulate each other’s expression while imparing cardiomyogenesis. Lastly, we show that Gli2 and MEF2C form a protein complex, which synergistically activates cardiac muscle related promoters. In Chapter 4, we illustrate that Gli2 associates with MyoD gene elements while enhancing skeletal myogenesis in P19 cells and activates the MyoD promoter in vitro. Furthermore, inhibition of Hh signalling in muscle satellite cells and in proliferating myoblasts leads to reduction in MyoD and MEF2C expression. Finally, we demonstrate that endogenous Hh signalling is important for MyoD transcriptional activity and that Gli2, MEF2C and MyoD form a protein complex capable of inducing skeletal muscle-specific gene expression. Thus, Gli2, MEF2C and MyoD participate in a regulatory loop and form a protein complex capable of inducing skeletal muscle-specific gene expression. Our results provide a link between the regulation of tissue-restricted factors like Mash1, MEF2C and MyoD, and a general signal-regulated Gli2 transcription factor. We therefore provide novel mechanistic insights into the neurogenic, cardiogenic and myogenic properties of Gli2 in vitro, and offer novel plausible explanations for its in vivo functions. These results may also be important for the development of stem cell therapy strategies.
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Fair, Joel Vincent. "Gli2 Accelerates Cardiac Progenitor Gene Expression During Mouse Embryonic Stem Cell Differentiation". Thesis, Université d'Ottawa / University of Ottawa, 2014. http://hdl.handle.net/10393/31579.

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The Hedgehog (HH) signalling pathway and its primary transducer, GLI2, regulate cardiomyogenesis in vivo and in differentiating P19 embryonal carcinoma (EC) cells. To further assess the role of HH signalling during mouse embryonic stem (mES) cell differentiation, we studied the effects of GLI2 overexpression during mES cell differentiation. GLI2 overexpression resulted in temporal enhancement of cardiac progenitor genes, Mef2c and Nkx2-5, along with enhancement of Tbx5, Myhc6, and Myhc7 in day 6 differentiating mES cells. Mass spectrometric analysis of proteins that immunoprecipitate with GLI2 determined that GLI2 forms a complex with BRG1 during mES cell differentiation. Furthermore, modulation of HH signalling during P19 EC cell differentiation followed by chromatin immunoprecipitation with an anti-BRG1 antibody determined that HH signalling regulates BRG1 enrichment on Mef2c. Therefore, HH signalling accelerates cardiac progenitor gene expression during mES cell differentiation potentially by recruiting a chromatin remodelling factor to at least one cardiac progenitor gene.
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日高, 京子, Kyoko Hidaka, 佳子 三輪, Keiko Miwa, 豊明 室原, Toyoaki Murohara, 謙次 笠井 i in. "Paracrine factors of vascular endothelial cells facilitate cardiomyocyte differentiation of mouse embryonic stem cells". Elsevier, 2008. http://hdl.handle.net/2237/10608.

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Części książek na temat "Cardiomyogenesis"

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Bylund, Jeffery B., i Antonis K. Hatzopoulos. "Directed Cardiomyogenesis of Pluripotent Stem Cells". W Chemical Biology in Regenerative Medicine, 15–33. Chichester, UK: John Wiley & Sons, Ltd, 2014. http://dx.doi.org/10.1002/9781118695746.ch2.

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Sato, Mariko, i H. Joseph Yost. "Neural Crest Cells Contribute to Heart Formation and Cardiomyogenesis in Zebrafish". W Cardiovascular Development and Congenital Malformations, 150–52. Malden, Massachusetts, USA: Blackwell Publishing Ltd, 2007. http://dx.doi.org/10.1002/9780470988664.ch38.

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Gutkowska, Jolanta, i Marek Jankowski. "Oxytocin as an Inducer of Cardiomyogenesis". W Embryonic Stem Cells: The Hormonal Regulation of Pluripotency and Embryogenesis. InTech, 2011. http://dx.doi.org/10.5772/14765.

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Franco, Diego, Estefania Lozano-Velasco i Amelia Araneg. "Transcriptional Networks of Embryonic Stem Cell-Derived Cardiomyogenesis". W Embryonic Stem Cells - Differentiation and Pluripotent Alternatives. InTech, 2011. http://dx.doi.org/10.5772/24459.

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Hao, Jijun, Li Zhou i Charles C. "Chemical Biology of Pluripotent Stem Cells: Focus on Cardiomyogenesis". W Embryonic Stem Cells - Recent Advances in Pluripotent Stem Cell-Based Regenerative Medicine. InTech, 2011. http://dx.doi.org/10.5772/16216.

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Streszczenia konferencji na temat "Cardiomyogenesis"

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Teo, Ailing, Amir Morshedi, Jen-Chieh Wang, Mayasari Lim i Yufeng Zhou. "Enhancement of cardiomyogenesis in stem cells by low intensity pulsed ultrasound". W PROCEEDINGS FROM THE 14TH INTERNATIONAL SYMPOSIUM ON THERAPEUTIC ULTRASOUND. Author(s), 2017. http://dx.doi.org/10.1063/1.4977671.

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Możesz być także zainteresowany rozszerzonymi bibliografiami na temat „Cardiomyogenesis” dla poszczególnych typów źródeł:
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