Relevant bibliographies by topics / Heart – Differentiation

Academic literature on the topic 'Heart – Differentiation'

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Published: 4 June 2021
Last updated: 13 February 2022

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Journal articles on the topic "Heart – Differentiation"

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Hildick-Smith, D. J. R. "Echocardiographic differentiation of pathological and physiological left ventricular hypertrophy." Heart 85, no. 6 (June 1, 2001): 615–19. http://dx.doi.org/10.1136/heart.85.6.615.

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Kempf, Tibor, and Kai C. Wollert. "Growth-Differentiation Factor-15 in Heart Failure." Heart Failure Clinics 5, no. 4 (October 2009): 537–47. http://dx.doi.org/10.1016/j.hfc.2009.04.006.

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Chen, J. N., and M. C. Fishman. "Zebrafish tinman homolog demarcates the heart field and initiates myocardial differentiation." Development 122, no. 12 (December 1, 1996): 3809–16. http://dx.doi.org/10.1242/dev.122.12.3809.

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The fashioning of a vertebrate organ requires integration of decisions of cell fate by individual cells with those that regulate organotypic form. Logical candidates for this role, in an organ such as the heart, are genes that initiate the differentiation process leading to heart muscle and those that define the earliest embryonic heart field, but for neither class are genes defined. We cloned zebrafish Nkx2.5, a homolog of the tinman homeodomain gene needed for visceral and cardiac mesoderm formation in Drosophila. In the zebrafish, its expression is associated with cardiac precursor cells throughout development, even in the early gastrula, where the level of zebrafish Nkx2.5 is in a gradient which spatially matches the regional propensity of ventral-marginal cells to become heart. Overexpression of Nkx2.5 causes formation of disproportionally larger hearts in otherwise apparently normal embryos. Transplanted cell expressing high levels of Nkx2.5 express cardiac genes even in ectopic locales. Fibroblasts transfected with myc-tagged Nkx2.5 express cardiac genes. These effects require the homeodomain. Thus, Nkx2.5 appears to mark the earliest embryonic heart field and to be capable of initiating the cardiogenic differentiation program. Because ectopic cells or transfected fibroblasts do not beat, Nkx2.5 is likely to be but one step in the determination of cardiac myocyte cell fate. Its overexpression increases heart size, perhaps by bringing cells on the edge of the field to a threshold level for initiation of cardiac differentiation.
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Davis, L. A., and L. F. Lemanski. "Induction of myofibrillogenesis in cardiac lethal mutant axolotl hearts rescued by RNA derived from normal endoderm." Development 99, no. 2 (February 1, 1987): 145–54. http://dx.doi.org/10.1242/dev.99.2.145.

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A strain of axolotl, Ambystoma mexicanum, that carries the cardiac lethal or c gene presents an excellent model system in which to study inductive interactions during heart development. Embryos homozygous for gene c contain hearts that fail to beat and do not form sarcomeric myofibrils even though muscle proteins are present. Although they can survive for approximately three weeks, mutant embryos inevitably die due to lack of circulation. Embryonic axolotl hearts can be maintained easily in organ culture using only Holtfreter's solution as a culture medium. Mutant hearts can be induced to differentiate in vitro into functional cardiac muscle containing sarcomeric myofibrils by coculturing the mutant heart tube with anterior endoderm from a normal embryo. The induction of muscle differentiation can also be mediated through organ culture of mutant heart tubes in medium ‘conditioned’ by normal anterior endoderm. Ribonuclease was shown to abolish the ability of endoderm-conditioned medium to induce cardiac muscle differentiation. The addition of RNA extracted from normal early embryonic anterior endoderm to organ cultures of mutant hearts stimulated the differentiation of these tissues into contractile cardiac muscle containing well-organized sarcomeric myofibrils, while RNA extracted from early embryonic liver or neural tube did not induce either muscular contraction or myofibrillogenesis. Thus, RNA from anterior endoderm of normal embryos induces myofibrillogenesis and the development of contractile activity in mutant hearts, thereby correcting the genetic defect.
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Kazez, A., I. H. Özercan, and P. S. Erol. "Sacrococygeal heart: a very rare differentiation in teratoma." Journal of Pediatric Surgery 38, no. 6 (June 2003): 990. http://dx.doi.org/10.1016/s0022-3468(03)00142-8.

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Kirkpatrick, Michael A., and Andrew S. Groves. "Verbal Feedback Facilitates Heart Rate Discrimination and Differentiation." European Journal of Behavior Analysis 12, no. 2 (December 2011): 431–39. http://dx.doi.org/10.1080/15021149.2011.11434393.

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Kazez, A., İ. H. Özercan, F. S. Erol, M. Faik Özveren, and E. Parmaksız. "Sacrococcygeal Heart: A Very Rare Differentiation in Teratoma." European Journal of Pediatric Surgery 12, no. 4 (August 2002): 278–80. http://dx.doi.org/10.1055/s-2002-34483.

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THOMPSON, R. P., J. R. LINDROTH, A. J. ALLES, and A. R. FAZEL. "Cell Differentiation Birthdates in the Embryonic Rat Heart." Annals of the New York Academy of Sciences 588, no. 1 Embryonic Ori (April 1990): 446–48. http://dx.doi.org/10.1111/j.1749-6632.1990.tb13259.x.

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Chen, Wei-Qian, Chuanfu Li, Hai-Bin Ruan, Xuan Jiang, Xin Qi, and Xiang Gao. "Myeloid Differentiation Protein-88 Signaling Mediates Heart Failure." Journal of Cardiac Failure 13, no. 6 (August 2007): S79. http://dx.doi.org/10.1016/j.cardfail.2007.06.395.

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Drenckhahn, Jörg-Detlef. "Heart Development: Mitochondria in Command of Cardiomyocyte Differentiation." Developmental Cell 21, no. 3 (September 2011): 392–93. http://dx.doi.org/10.1016/j.devcel.2011.08.021.

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Dissertations / Theses on the topic "Heart – Differentiation"

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Litster, Caroline Elizabeth. "Heart rate, heart rate variability, electrodermal activity and the differentiation-of-deception /." Title page, table of contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09SSPS/09sspsl7769.pdf.

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Hinds, Heather C. "Evaluating terminal differentiation of porcine valvular interstitial cells in vitro." Link to electronic thesis, 2006. http://www.wpi.edu/Pubs/ETD/Available/etd-050506-113014/.

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O'Brien, Meghan M. "A pilot proteomic analysis : the study of P19 cells in cardiac differentiation /." Connect to resource online, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=ysu1229374725.

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Buccini, Stephanie M. "Cardiogenic differentiation of induced pluripotent stem cells for regeneration of the ischemic heart." University of Cincinnati / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1382373160.

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Younce, Craig. "Zinc-Finger Protein MCPIP in Cell Death and Differentiation." Doctoral diss., University of Central Florida, 2009. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/2279.

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Monocyte chemotactic protein-1 (MCP-1) plays a critical role in the development of cardiovascular diseases. How MCP-1 contributes to the development of heart disease is not understood. We present evidence that MCP-1 causes death in cardiac myoblasts, H9c2 by inducing oxidative stress, ER stress and autophagy via a novel Zn-finger protein, MCP-1 induced protein (MCPIP). MCPIP expression caused cell death and knockdown of MCPIP, attenuated MCP-1 induced cell death. Expression of MCPIP resulted in induction of iNOS and production of reactive oxygen (ROS). It caused induction of NADPH oxidase subunit phox47 and its translocation to the cytoplasmic membrane. Oxidative stress led to the induction of ER stress markers HSP40, PDI, GRP78 and IRE1α. ER stress lead to autophagy as indicated by beclin-1 induction, cleavage of LC3 to LCII and autophagolysosome formation. Here, MCPIP-induced processes lead to apoptosis as indicated by caspase 3 activation and TUNEL assay. This cell death involved caspase 2 and caspase 12 as specific inhibitors of these caspases prevented MCPIP-induced cell death. Inhibitors of oxidative stress inhibited ER stress, and cell death. Specific inhibitors of ER stress inhibited autophagy and cell death. Inhibition of autophagy inhibited cell death. Microarray analysis showed that MCPIP expression caused induction of a variety of genes known to be involved in cell death. MCPIP caused activation of JNK and p38 and induction of p53 and PUMA. These results collectively suggest that MCPIP induces ROS/RNS production that causes ER stress which leads to autophagy and apoptosis through caspase 2/12 and IRE1α –JNK/p38-p53-PUMA pathway. These results provide the first molecular insights into the mechanism by which elevated MCP-1 levels associated with chronic inflammation may contribute to the development of heart failure. A role for inflammation and MCP-1 in obesity and diabetes has been implicated. Adipogenesis is a key process involved in obesity and associated diseases such as type 2 diabetes. This process involves temporally regulated genes controlled by a set of transcription factors, C/EBPβ, C/EBPδ, C/EBPα, and PPARγ. Currently PPARγ is considered the master regulator of adipogenesis as no known factor can induce adipogenesis without PPARγ. We present evidence that a novel Zn-finger protein, MCPIP, can induce adipogenesis without PPARγ. Classical adipogenesis-inducing medium induces MCP-1 production and MCPIP expression in 3T3-L1 cells before the induction of the C/EBP family of transcription factors and PPARγ. Knockdown of MCPIP prevents their expression and adipogenesis. Treatment of 3T3-L1 cells with MCP-1 or forced expression of MCPIP induces expression of C/EBPβ, C/EBPδ, C/EBPα, PPARγ and adipogenesis without any other inducer. Forced expression of MCPIP induces adipogenesis in PPARγ-/- fibroblasts. Thus, MCPIP is a newly identified master controller that can induce adipogenesis without PPARγ. Heart failure is a major cause of death in diabetic patients. Hyperglycemia is a major factor associated with diabetes that causes cardiomyocyte apoptosis that leads to diabetic cardiomyopathy. Cardiomyoycte apoptosis is a key event involved in the pathophysiological progression of diabetic cardiomyopathy. We have recently found that in ischemic hearts, MCP-1 can induce the zinc-finger protein, MCP-1 induced protein (MCPIP) that causes cardiomyocyte apoptosis. Although there is evidence that inflammation may play a role in diabetic cardiomyopathy, the underlying mechanisms are poorly understood. In this study, we show that treatment of H9c2 cardiomyoblasts and Neonatal Rat Ventricular Myocytes (NRVM) with 28mmol/L glucose concentration results in the induction of both transcript and protein levels of MCP-1 and MCPIP. Inhibition of MCP-1 interaction with CCR2 via specific antibody or with the G-coupled receptor inhibitors propagermanium and pertussis toxin attenuated glucose-induced cell death. Knockdown of MCPIP with specific siRNA yielded similar results. Treatment of cells with 28mmol/L glucose resulted in increased ROS production and phox47 activation. Knockdown of MCPIP attenuated these effects. The increased ROS production observed in H9c2 cardiomyoblasts and NRVM’s resulted in increased ER stress proteins GRP78 and PDI. Knockdown of MCPIP attenuated expression of both GRP78 and PDI. Inhibition of ER stress with TUDC and 4’PBA prevented high glucose-induced cell death death. Treatment of cells with 28mmol/l glucose resulted in autophagy as determined by an increase in expression of beclin-1 and through increased cleavage of LC3I to LC3II. Knockdown of MCPIP attenuated expression of beclin-1 and prevented cleavage of LC3. Addition of the autophagy inhibitors 3’methyladenine and LY294002 attenuated high glucose-induced H9c2 cardiomyoblast death. We conclude that high glucose-induced H9c2 cardiomyoblast death is mediated via MCP-1 induction of MCPIP that results in ROS that leads to ER stress that causes autophagy and eventual apoptosis.
Ph.D.
Department of Biomolecular Science
Burnett College of Biomedical Sciences
Biomedical Sciences PhD
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Wei, Wenjie, and 魏闻捷. "Calcium signaling in the cardiac differentiation of mouse embryonic stem cells." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2012. http://hub.hku.hk/bib/B49617862.

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　　Intracellular Ca2+ mobilization via secondary messengers modulates multiple cell functions. Cyclic Adenosine 5’-Diphosphate-Ribose (cADPR) is one of the most well recognized endogenous Ca2+ mobilizing messengers. In mammalian, cADPR is mainly formed by CD38, a multi-functional enzyme, from nicotinamide adenine dinucleotide (NAD). It has previously been shown that the cADPR/CD38/Ca2+pathway mediates many cardiac functions, such as regulating the excitation-contraction coupling in cardiac myocytes and modulating the Ca2+ homeostasis during the ischemia injury of the heart. Thus it is reasonable to propose that the cADPR/CD38/Ca2+ pathway plays a role in cardiogenesis. The pluripotent mouse embryonic stem (mES) cells which can be induced to differentiate into all cell types provide an ideal model for studying cardiogenesis. The first part of this dissertation is to determine the role of CD38/cADPR/Ca2+pathwayin the cardiomyogenesis of mES cells. The data showed that CD38 expression was markedly up-regulated during the in vitro embryoid body (EB) differentiation of mouse ES cells, which indicated a regulatory role of CD38 in the differentiation process. Lentivirus mediated shRNA provides a convenient method to knockdown the expression of CD38 in mES cells. Surprisingly, beating clusters appeared earlier and more in CD38 knockdown EBs than that in control EBs. Likewise, the expressions of several cardiac markers were up regulated in CD38 knockdown EBs. In addition, more cardiomyocytes (CMs) existed in CD38 knockdown or 8-Br-cADPR, a cADPR antagonist, treated EBs than those in control EBs. On the other hand, over-expression of CD38 in mouse ES cells significantly inhibited CM differentiation. Moreover, we showed that CMs derived from the CD38 knock down mES cells possessed the functional properties characteristic of CMs derived fromnormal ES cells. Last, we showed that the CD38-cADPR pathway negatively modulated the FGF4-Erks1/2cascade during CM differentiation of mES cells, and transiently inhibition of Erk1/2 blocked the enhancive effects of CD38 knockdown on the differentiation of CM from mES cells. Taken together, our data indicate that the CD38/cADPR/Ca2+ signaling pathway suppresses the cardiac differentiation of mES cells. 　　One of the main goals of the researches on cardiac differentiation of ES cells is to enhance the production of CMs from ES cells, thereby providing sufficient amount of functional intact CMs for the treatment of severe heart disease. Nitric oxide (NO) has been found to be a powerful cardiogenesis inducer of mES cells, in that it can significantly increase the yield of ES-derived CM. The second objective of this dissertation is to explore the mechanism underlying the NO facilitated cardiomyogenesis of mES cells. We found that the NO did induce intracellular Ca2+ increases in mES cells, and this Ca2+ increase was due to internal Ca2+ release from ER through theIP3 pathway. Therefore, the expression of IP3 receptors (IP3Rs) in mES cells were knocked down by lentivirus-mediated shRNAs. Interestingly, only type 3 IP3R (IP3R3) knockdown significantly inhibited the NO induced Ca2+ release in mES cells. Moreover, NO facilitated cardiogensis of mES cells was abolished in IP3R3 knockdown EBs. In summary, our results indicate that the IP3R3-Ca2+ pathway is required for NO facilitated cardiomyogenesis of mES cells.
published_or_final_version
Physiology
Doctoral
Doctor of Philosophy
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Chau, Dinh Le Mary. "Role of Notch1 in Cardiac Cell Differentiation and Migration: A Dissertation." eScholarship@UMMS, 2007. https://escholarship.umassmed.edu/gsbs_diss/338.

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The cardiac conduction system is responsible for maintaining and orchestrating the rhythmic contractions of the heart. Results from lineage tracing studies indicate that precursor cells in the ventricles give rise to both cardiac muscle and conduction cells. Using chick embryonic hearts, we have found that Notch signaling plays an important role in the differentiation of cardiac muscle and conduction cell lineages in the ventricles. Notch1 expression coincides with a conduction marker at early stages of conduction system development. Mis-expression of constitutively active Notch1 (NIC) in early heart tubes exhibited multiple effects on cardiac cell differentiation. Cells expressing NIC had a significant decrease in the expression of cardiac muscle markers, but an increase in the expression of conduction cell markers. Loss-of-function studies further support that Notch1 signaling is important for the differentiation of these cardiac cell types. Functional electrophysiology studies show that the expression of constitutively active Notch1 resulted in abnormalities in ventricular conduction pathway patterns. During cardiogenesis, groups of myocardial cells become separated from each other, and migrate to form the trabeculae. These finger-like projections found within the ventricular chamber coalesce to generate the muscular portions of the interventricular septum, the thickened myocardium, and future sites of the conduction system. We have found that Notch signaling regulates the migration of cardiac cells during cardiogenesis. Over-expression of constitutively active Notch causes cells to localize more centrally within the heart, while loss-of-Notch function results in cells distributed within the periphery of the heart. Staining of heart sections shows that Notch signaling regulates the expression of N-cadherin, the predominant adhesion molecule in cardiomyocytes. We find that the effects of Notch on cell migration are two-fold: delamination and cell motility. Time-lapse studies demonstrate that Notch signaling increases cell motility, but does not affect speed or directionality of migration. Furthermore, we find that the effects of Notch on cell migration is independent of its effects on differentiation.
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Maliken, Bryan D. B. A. "Gata4-Dependent Differentiation of c-Kit+ Derived Endothelial Cells Underlies Artefactual Cardiomyocyte Regeneration in the Heart." University of Cincinnati / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1535375861364685.

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Huang, Tianfang. "Mechanism of Arsenical Toxicity on TGFβ Signaling and Genetic Regulation During Cardiac Progenitor Cell Differentiation." Diss., The University of Arizona, 2015. http://hdl.handle.net/10150/556428.

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Low to moderate level of chronic arsenic exposure contributes to cardiovascular ailments including heart disease and aneurysms. Current research on the etiology and progression of cardiovascular disease focuses mainly on adult which fails to capture the developmental origins of cardiovascular disease. Thus, disruption in morphogenetic events during early development may initiate and pattern the molecular programming of cardiovascular ailments in adulthood. A major contributor to ischemic heart pathologies is coronary artery disease, however the influences by environmental arsenic in this disease process are not known. Similarly, the impact of toxicants on blood vessel formation and function during development has not been studied. Coronary vessel development is initiated by precursor cells that are derived from the epicardium. Epicardial derived cells undergo proliferate, migrate, and differentiate into several cardiac cell types which are the cellular components of the coronary vessels. The key cellular event occurs in this process is the epithelial to mesenchymal transition (EMT), which can also be utilized by endocardial cushion cells to form aortic and pulmonary valves. The TGFβ family of ligands and receptors are essential for developmental cardiac EMT and coronary smooth muscle cell differentiation. Whether arsenic has any impact on TGFβ mediated cardiovasculogenesis is not known. Monomethylarsonous acid [MMA(III)] is the most potent metabolite of inorganic arsenic and has been shown to partly account for arsenic induced toxicity. The fetus is exposed to relatively higher levels of MMA (III) as compared to adults probably due to deficiency in methylation of transferred inorganic arsenic from the placenta. However, the developmental toxicity of MMA (III) has not yet been studied. In this study, we exploit a novel cardiac progenitor cell line to recapitulate epicardial EMT in vitro and to study developmental toxicity caused by arsenicals. We show that chronic exposure to low level of arsenite and MMA (III) disrupts developmental EMT programming in epicardial cells causing deficits in cardiac mesenchyme production. The expression of EMT program genes is also decreased in a dose-dependent manner following exposure to arsenite and MMA (III). Smad-dependent TGFβ2 canonical signaling and the non-canonical Erk signaling pathways are abrogated as detected by decreases in phosphorylated Smad2/3, Erk1/2 and Erk5 proteins. There is also loss of nuclear accumulation of p-Smad and p-Erk5 due to arsenical exposure. These observations coincide with a decrease in vimentin positive mesenchymal cells invading three-dimensional collagen gels. However, arsenicals do not block TGFβ2 stimulated p38 activation. Additionally, smooth muscle cell differentiation, which is proven to be governed by p38 signaling in epicardial cells, also remains intact with arsenical exposure. Overall these results show that arsenite and MMA (III) are strong and selective cardiac silencers. The molecular mechanisms of arsenical toxicity on TGFβ-Smad signaling in epicardial cells is further explored. A relatively high level of acute arsenical exposure rapidly depletes phosphorylated nuclear Smad2/3. Restoration of the nuclear accumulation of Smads can be achieved by inhibiting the expression or activation of Smad specific exportins suggesting that arsenicals augment Smad nuclear exportation. Abrogated Smad signaling caused by arsenicals is associated with severe deficits in EMT during mouse epicardium and chick endocardial cushion development. Thus progenitor cell outgrowth, migration, invasion and vimentin filament reorganization are significantly inhibited in response to arsenical exposure. Disrupted Smad nuclear shuffling is probably caused by zinc displacement on the MH-1 DNA binding domain of Smad2/3. Thus zinc supplementation restores both nuclear content and transcriptional activities of Smad2/3. Rescued TGFβ-Smad signaling by zinc also contributes to cellular transformation and mesenchyme production in embryonic heart explants. LINE1 (L1) retrotransposons are a group of mobile DNA elements that shape the genome via novel epigenetic controls. Although expression of L1 is required for early embryo implantation and development, abnormally elevated L1 is shown to inhibit embryonic cells from transforming and differentiating during organogenesis. Cellular redox signaling, which is regulated by antioxidant responsive elements (AREs), has been shown to play a key role in L1 activation and retrotransposition. However, whether L1 can be induced by the cellular oxidative stress caused by arsenic is not known. We provide evidence showing that L1 ORF-1 and ORF-2 mRNA levels are both up-regulated by arsenic. Nuclear accumulation of L1 ORF-2 is observed in response to 30 min arsenic exposure, which may lead to active retrotransposition events in the genome. Transcriptional activity of L1 is regulated by Nrf2 as mutations in ARE regions within the L1 promoter and Nrf2 silencing using siRNA both significantly inhibit L1 transcriptional activity. Nrf2 overexpression together with arsenic exposure creates synergic induction in L1 promoter activity suggesting that arsenic mediated L1 activation is partially Nrf2 dependent. Taken together, these findings reveal a molecular mechanism responsible for arsenic cardiac toxicity and define a novel genetic toxic effect of arsenic during embryonic heart development.
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Momtahan, Nima. "Extracellular Matrix from Whole Porcine Heart Decellularization for Cardiac Tissue Engineering." BYU ScholarsArchive, 2016. https://scholarsarchive.byu.edu/etd/6225.

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Heart failure is one of the leading causes of death in the United States. Every year in the United States, more than 800,000 people are diagnosed with heart failure and more than 375,000 people die from heart disease. Current therapies such as heart transplants and bioartificial hearts are helpful, but not optimal. Decellularization of porcine whole hearts followed by recellularization with patient-specific human cells may provide the ultimate solution for patients with heart failure. Great progress has been made in the development of efficient processes for decellularization, and the design of automated bioreactors. In this study, the decellularization of porcine hearts was accomplished in 24 h with only 6 h of sodium dodecyl sulfate (SDS) exposure and 98% DNA removal. Automatically controlling the pressure during decellularization reduced the detergent exposure time while still completely removing immunogenic cell debris. Stimulation of macrophages was greatly reduced when comparing native tissue samples to the processed ECM. Complete cell removal was confirmed by analysis of DNA content. General collagen and elastin preservation was demonstrated by SEM and histology. The compression elastic modulus of the ECM after decellularization was lower than native at low strains but there was no significant difference at high strains. Polyurethane casts of the vasculature of native and decellularized hearts demonstrated that the microvasculature network was preserved after decellularization. A static blood thrombosis assay using bovine blood was also developed. A perfusion bioreactor was designed and right ventricle of the decellularized hearts were recellularized with human endothelial cells and cardiac fibroblasts. An effective, reliable, and relatively inexpensive assay based on human blood hemolysis was developed for determining the remaining cytotoxicity of the cECM and the results were consistent with a standard live/dead assay using MS1 endothelial cells incubated with the cECM. Samples from the left ventricle of the hearts were prepared with 300 µm thickness, mounted on 10 mm round glass coverslips. Human induced pluripotent stem cells were differentiated into cardiomyocytes (CMs) and 4 days after differentiation, cardiac progenitors were seeded onto the decellularized cardiac slices. After 10 days, the tissues started to beat spontaneously. Immunofluorescence images showed confluent coverage of CMs on the decellularized slices and the effect of the scaffold was evident in the arrangement of the CMs in the direction of fibers. This study demonstrated the biocompatibility of decellularized porcine hearts with human CMs and the potential of these scaffolds for cardiac tissue engineering. Further studies can be directed toward 3D perfusion recellularization of the hearts and improving repopulation of the scaffolds with various cell types as well as adding mechanical and electrical stimulations to obtain more mature CMs.
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Books on the topic "Heart – Differentiation"

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J, Hearse David, ed. The developing myocardium. Mt. Kisco, NY: Futura Pub. Co., 1991.

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Cell cycle regulation and differentiation in cardiovascular and neural systems. New York: Springer, 2010.

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Watson, Andrea. Heat shock proteins in leukaemia cell differentiation and cell death. Birmingham: Aston University. Departmentof Pharmaceutical Sciences, 1990.

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Lesuisse, Christian. Role of the constitutive heat shock portein HSC70 during differentiation of haemopoieticcells. Manchester: University of Manchester, 1994.

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B, Clark Edward, Markwald Roger R, and Takao Atsuyoshi, eds. Developmental mechanisms of heart disease. Armonk, NY: Futura Pub., 1995.

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De la Cruz, María Victoria. and Markwald Roger R, eds. Living morphogenesis of the heart. Boston: Birkhäuser, 1998.

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B, Clark Edward, and Takao Atsuyoshi, eds. Developmental cardiology: Morphogenesis and function. Mount Kisco, N.Y: Futura Pub. Co., 1990.

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Takao, Atsuyoshi, and Edward Clark. Developmental Cardiology: Morphogenesis and Function. Futura Pub Co, 1990.

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Giordano, Antonio, and Umberto Galderisi. Cell Cycle Regulation and Differentiation in Cardiovascular and Neural Systems. Springer, 2014.

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van den Hoff, Maurice J. B., and Antoon F. M. Moorman. From heart-forming region to ballooning chambers. Edited by Miguel Torres. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198784906.003.0006.

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This chapter describes the formation of the adult four-chambered heart from the precardiac mesodermal cells. The precardiac mesoderm develops into a linear heart tube by the process of folding. The subsequent increase in size of the heart by the addition of precursor cells derived from the first and second heart fields is discussed. For the sake of clarity, the chapter describes the addition of precursor cells to the inflow and outflow, separately. Next, the formation of the ventricular chambers with respect to ballooning and differentiation into a compact and trabecular layer is discussed. Finally, the formation of the septa in the heart tube is described, creating the adult four-chambered heart.
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Book chapters on the topic "Heart – Differentiation"

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Makino, Shinji, and Keiichi Fukuda. "Methods for Differentiation of Bone-Marrow-Derived Stem Cells into Myocytes." In Regenerating the Heart, 67–81. Totowa, NJ: Humana Press, 2011. http://dx.doi.org/10.1007/978-1-61779-021-8_6.

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Lescroart, Fabienne, and Sigolène M. Meilhac. "Cell Lineages, Growth and Repair of the Mouse Heart." In Results and Problems in Cell Differentiation, 263–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-30406-4_15.

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Linask, Kérsti K. "Regulatory Role of Cell Adhesion Molecules in Early Heart Development." In Formation and Differentiation of Early Embryonic Mesoderm, 301–13. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3458-7_24.

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Rajamannan, Nalini M., Muzaffer Cicek, John R. Hawse, Thomas C. Spelsberg, and Malayannan Subramaniam. "Experimental Model of Aortic Valve Calcification to Induce Osteoblast Differentiation." In Molecular Biology of Valvular Heart Disease, 27–33. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6350-3_4.

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Rajamannan, Nalini M. "Ex Vivo Model for Bioprosthetic Valve Calcification via Stem Cell Differentiation to Bone." In Molecular Biology of Valvular Heart Disease, 49–54. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6350-3_7.

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Müller, Mathias M., Helmut RumpoId, Gerhard Schopf, and Peter Zilla. "Changes of Purine Metabolism During Differentiation of Rat Heart Myoblasts." In Purine and Pyrimidine Metabolism in Man V, 475–84. New York, NY: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-1248-2_74.

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Osmond, Mark. "The Effects of Retinoic Acid on Early Heart Formation and Segmentation in the Chick Embryo." In Formation and Differentiation of Early Embryonic Mesoderm, 275–300. Boston, MA: Springer US, 1992. http://dx.doi.org/10.1007/978-1-4615-3458-7_23.

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Hiraumi, Yoshimi, Chengqun Huang, Allen M. Andres, Ying Xiong, Jennifer Ramil, and Roberta A. Gottlieb. "Myogenic Progenitor Cell Differentiation Is Dependent on Modulation of Mitochondrial Biogenesis through Autophagy." In Etiology and Morphogenesis of Congenital Heart Disease, 127–28. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-54628-3_15.

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Rajamannan, Nalini M., Muzaffer Cicek, John R. Hawse, Thomas C. Spelsberg, and Malayannan Subramaniam. "In Vitro Cell Culture Model of Calcification: Molecular Regulation of Myofibroblast Differentiation to an Osteoblast Phenotype." In Molecular Biology of Valvular Heart Disease, 13–20. London: Springer London, 2014. http://dx.doi.org/10.1007/978-1-4471-6350-3_2.

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Sato, Yohei, Takashi Higuchi, Hiroshi Kobayashi, Susumu Minamisawa, Hiroyuki Ida, and Toya Ohashi. "Lentiviral Gene Transfer to iPS Cells: Toward the Cardiomyocyte Differentiation of Pompe Disease-Specific iPS Cells." In Etiology and Morphogenesis of Congenital Heart Disease, 341–43. Tokyo: Springer Japan, 2016. http://dx.doi.org/10.1007/978-4-431-54628-3_48.

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Conference papers on the topic "Heart – Differentiation"

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Hacke, M., J. Signoret-Genest, P. Tovote, and M. Romanos. "Definition, detection and differentiation of acute emotional states using heart rate recording." In Abstracts of the 2nd Symposium of the Arbeitsgemeinschaft für Neuropsychopharmakologie und Pharmakopsychiatrie (AGNP) and Deutsche Gesellschaft für Biologische Psychiatrie (DGBP). Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0039-3403003.

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Yi, Wei-guo, Ming-yu Lu, Zhi Liu, and Hao Xu. "Association Rule Discovery with Fuzzy Decreasing Support on Syndrome Differentiation in Coronary Heart Disease." In 2009 2nd International Conference on Biomedical Engineering and Informatics. IEEE, 2009. http://dx.doi.org/10.1109/bmei.2009.5304789.

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Young, Jennifer L., Kyle Kretchmer, and Adam J. Engler. "Temporally-Stiffening Hydrogel Regulates Cardiac Differentiation via Mechanosensitive Signaling." In ASME 2013 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/sbc2013-14674.

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Stiffness of the extracellular matrix (ECM) surrounding cells plays an integral role in affecting how a cell spreads, migrates, and differentiates, in the case of stem cells. For mature cardiomyocytes, stiffness regulates myofibril striation, beating rate, and fiber alignment, but does not induce de-differentiation [1,2]. Despite improved myocyte function on materials which mimic the ∼10 kPa heart stiffness, the heart does not begin as a contractile ∼10 kPa material, but instead undergoes ∼10-fold myocardial stiffening during development [3]. Thiolated hyaluronic acid (HA) hydrogels have been used to mimic these stiffening dynamics by varying hydrogel functionality and component parameters. Recently, we have shown that pre-cardiac mesodermal cells plated on top of these stiffening HA hydrogels improves cardiomyocyte maturation compared to static, compliant polyacrylamide (PA) hydrogels [3]. While active mechanosensing causes maturation, the specific mechanisms responsible for responding to time-dependent stiffness remain unknown. Here we examined protein kinase signaling and mechanics in response to dynamic vs. static stiffness during the commitment process from embryonic stem cells (ESCs) through cardiomyocytes to better understand how developmentally-appropriate temporal changes in stiffness regulate cell commitment.
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Yi, Weiguo, Jing Duan, and Mingyu Lu. "Association rule discovery with fuzzy decreasing support on Syndrome Differentiation and medication in coronary heart disease." In 2010 3rd International Conference on Biomedical Engineering and Informatics (BMEI). IEEE, 2010. http://dx.doi.org/10.1109/bmei.2010.5639351.

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Argento, G., M. Simonet, C. W. J. Oomens, and F. P. T. Baaijens. "Mechanics of Electrospun Scaffolds: An Application to Heart Valve Tissue Engineering." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80724.

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In the last decade electrospinning has shown its potential of being a feasible technique to manufacture scaffolds for tissue engineering [1]. Previous studies observed that, on a micrometer scale, the topology of the scaffold plays a fundamental role in the spreading and the differentiation of the cells [2], and in the growth of neo-extracellular matrix. On a tissue scale (in the order of cm) the stiffness of the construct enables the possibility of applying mechanical cues for the development of a functional engineered tissue [3]. Studies on scaffold mechanics based on volume-averaging theory succeeded in demonstrating that the arrangement of the micro-scale scaffold components influences the macro-scale mechanical behavior [4].
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Salinas, M., R. Lange, and S. Ramaswamy. "Specimen Dynamics and Subsequent Implications in Heart Valve Tissue Engineering Studies." In ASME 2011 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2011. http://dx.doi.org/10.1115/sbc2011-53346.

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In heart valve tissue engineering, appropriate mechanical preconditioning may provide the necessary stimuli to promote proper tissue formation [1–3]. Previous efforts have focused on a mechanistic heart valve (MHV) bioreactor that can mimic the innate mechanical stress states of flexure, flow and stretch in any combination thereof [1]. A fundamental component pertaining to heart valves is its dynamic behavior. Specific fluid-induced shears stress patterns may play a critical role in up-regulating ECM secretion by progenitor cell sources such as bone marrow derived stem cells [2] and increasing the possibility of cell differentiation towards a heart valve phenotype. Here, we take a computational predictive modeling approach to identify the specific fluid induced shear stress distributions that are altered as a result of valve-like movement and its resulting implications for tissue growth. Previous results have demonstrated the analogous deformation characteristics of heart valves in a rectangular geometry [2]. We conducted computational fluid dynamic (CFD) simulations of a bioreactor that houses these rectangular-shaped specimens (Fig.1).
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Varner, Victor D., and Larry A. Taber. "Not Just Inductive: A Critical Mechanical Role for the Endoderm During Heart Tube Assembly." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80621.

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The heart is the first functioning organ to form during development. Similar to other organ primordia, the embryonic heart forms as a simple tube — in this case, a straight muscle-wrapped tube situated on the ventral side of the embryo. During gastrulation, the cardiac progenitors reside in the lateral plate mesoderm but maintain close contact with the underlying endoderm. In amniotes, these bilateral heart fields are initially organized as a pair of flat epithelia that move toward the embryonic midline and fuse above the anterior intestinal portal (AIP) to form the heart tube. This medial motion is typically attributed to active mesodermal migration over the underlying endoderm. In this view, the role of the endoderm is two-fold: to serve as a mechanically passive substrate for the crawling mesoderm and to secrete various growth factors necessary for cardiac specification and differentiation.
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Salinas, M., D. Schmidt, R. Lange, M. Libera, and S. Ramaswamy. "Computational Prediction of Fluid Induced Stress States in Dynamically Conditioned Engineered Heart Valve Tissues." In ASME 2012 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/sbc2012-80787.

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There is extensive documented evidence that mechanical conditioning plays a significant role in the development of tissue grown in-vitro for heart valve scaffolds [1–3]. Modern custom made bioreactors have been used to study the mechanobiology of engineered heart valve tissues [1]. Specifically fluid-induced shears stress patterns may play a critical role in up-regulating extracellular matrix secretion by progenitor cell sources such as bone marrow derived stem cells (BMSCs) [2] and increasing the possibility of cell differentiation towards a heart valve phenotype. We hypothesize that specific biomimetic fluid induced shear stress environments, particularly oscillatory shear stress (OSS), have significant effects on BMSCs phenotype and formation rates. As a first step here, we attempt to quantify and delineate the entire 3-D flow field by developing a CFD model to predict the fluid induced shear stress environments on engineered heart valves tissue under quasi-static steady flow and dynamic steady flow conditions.
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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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Lahm, H., F. Wirth, M. Dreßen, M. Jia, N. Puluca, J. Cleuziou, S. Doppler, R. Lange, B. Müller-Myhsok, and M. Krane. "Functional Analysis of Candidate Genes Associated with Congenital Heart Disease during Differentiation of Induced Pluripotent Stem Cells and in the Human Embryonic and Adult Heart at Single-Cell Resolution." In 50th Annual Meeting of the German Society for Thoracic and Cardiovascular Surgery (DGTHG). Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1725667.

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