Journal articles: 'Heart – Differentiation'

1

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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9

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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Rugendorff, Astrid, Amelia Younossi-Hartenstein, and Volker Hartenstein. "Embryonic origin and differentiation of the Drosophila heart." Roux's Archives of Developmental Biology 203, no. 5 (March 1994): 266–80. http://dx.doi.org/10.1007/bf00360522.

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12

Patanè, Salvatore. "Growth Differentiation Factor-15 in Chronic Heart Failure." JACC: Heart Failure 6, no. 2 (February 2018): 177. http://dx.doi.org/10.1016/j.jchf.2017.10.013.

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13

Voronina, L. P., O. S. Polunina, O. A. Bashkina, E. A. Polunina, and T. V. Prokofieva. "Phenotypic differentiation of patients with chronic heart failure." Medical alphabet, no. 36 (January 13, 2021): 28–33. http://dx.doi.org/10.33667/2078-5631-2020-36-28-33.

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Objective. According to the results of a complex analysis of gender-anamnestic, clinical, biochemical and instrumental parameters using the cluster analysis method to identify phenotypes of chronic heart failure (CHF) in the examined patients.Materials and methods. It was examined 345 patients with CHF with different left ventricular ejection fraction and 60 somatically healthy volunteers. For the study, groups of indicators were formed that most widely characterize the pathogenesis of CHF: gender-anamnestic and clinical, instrumental (echocardiographic study, study of the functional state of the vascular endothelium and skin microcirculation, calculation of the volume fraction of interstitial collagen), biochemical parameters of the functional state of the vascular endothelium, collagen balance, inflammation and oxidative stress.Results. After the cluster analysis by the methods of hierarchical classification and k-means, we identified 4 clusters/phenotypes of CHF: fibrous-rigid, fibrous-inflammatory, inflammatory-destructive and dilatation-maladaptive. According to the results of the analysis of variance were identified 27 of the 48 indicators in which the level of statistical significance of intergroup differences (for the Fisher test) was less than 0.05, that is, indicators that make the greatest contribution to the division of patients with CHF into phenotypic groups.Conclusion. Our analysis with the release of phenotypes indicates that patients with CHF with different phenotypes have clinical and pathogenetic features. The data obtained in the future can be used to determine the prognosis of the disease and the choice of tactics for the management and treatment of patients with CHF depending on the phenotype.

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Chang, Yuqiao, Kang Guo, Qiong Li, Cixia Li, Zhikun Guo, and He Li. "Multiple Directional Differentiation Difference of Neonatal Rat Fibroblasts from Six Organs." Cellular Physiology and Biochemistry 39, no. 1 (2016): 157–71. http://dx.doi.org/10.1159/000445613.

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Background/Aims: Fibroblasts are abundantly distributed throughout connective tissues in the body and are very important in maintaining the structural and functional integrity. Recent reports have proved that fibroblasts and mesenchymal stem cells share much more in common than previously recognized. The aim of this study was to investigate comparative studies in fibroblasts on the differences in the expression of molecular markers and differentiation capacity from different organs. Methods: Combined trypsin/collagenase enzymes digestion method was used to isolate and culture the fibroblasts derived from heart, liver, spleen, lung, kidney and skin. Cell activity was determined by methyl thiazolyl tetrazolium (MTT) assay. Common molecular markers for fibroblasts such as vimentin, DDR2 and FSP1, stem cell markers nanog, c-kit and sca-1 were detected by RT-PCR, immunofluorescence and western blotting. The osteogenic, adipogenic and cardiogenic differentiations of fibroblasts were performed by inductive culture in special mediums, and analyzed by Alizarin red, Oil red O and immunofluorescence staining of cTnT respectively. Results: The proliferation rate of fibroblasts in lung was faster than in other five organs. Common molecular markers for fibroblasts were expressed differently in different organs. DDR2 was strongly expressed in fibroblasts in the heart, partly expressed in the heart, skin, liver and spleen. Interestingly, no expression of DDR2 was detected in liver and kidney. However, vimentin and FSP1 were consistently expressed in fibroblasts from skin, liver, kidney, spleen and lung. nanog expression in fibroblasts from lung was less than that from heart, skin, liver and spleen (P < 0.01). c-kit expression in fibroblasts from heart, skin and kidney was higher than that from spleen (P < 0.05), while the c-kit positive fibroblasts from liver was obviously higher than that from spleen (P < 0.01). But sca-1 expression in fibroblasts from lung was the lowest among six organs (P < 0.01). Directed differentiation in vitro had demonstrated that skin fibroblasts had the strongest multiple differentiation potential, and the next was cardiac fibroblasts. And fibroblasts in liver and kidney had the advantage in myocardial differentiation, while fibroblasts in spleen only had the advantage in osteogenic differentiation. Conclusions: There are obvious heterogeneity in molecular markers and muti-directional differentiation in fibroblasts from six organs.

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15

Canale, E., J. J. Smolich, and G. R. Campbell. "Differentiation and innervation of the atrioventricular bundle and ventricular Purkinje system in sheep heart." Development 100, no. 4 (August 1, 1987): 641–51. http://dx.doi.org/10.1242/dev.100.4.641.

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The development of the atrioventricular bundle (AVB) and ventricular Purkinje system and their innervation have been studied in fetal sheep from 27 to 140 days gestation (term is 147 days). The AVB initially consisted of a primordium, which lacked innervation and was composed of small, relatively undifferentiated myocytes. Differentiation of Purkinje-like cells within the AVB began near its distal end and extended towards the atrioventricular node (AVN). Differentiation of the ventricular Purkinje system extended distally from the region of bifurcation of the AVB from cells that were indistinguishable from the working myocardium and continuous with the AVB primordium. Differentiation of Purkinje-like AVB cells was complete by 46 days gestation but Purkinje fibres were still differentiating within the ventricular wall at 60 days gestation. The main morphological changes included a large increase in cell size and organization into strands, development of characteristic glycogen-filled regions containing many intermediate filaments and early development of myofibrillar M lines compared to the working myocardium. The differentiation of AVB cells and the ventricular Purkinje system preceded their innervation. The AVB became innervated earlier than ventricular Purkinje fibres, intimate contacts between proximal AVB cells and nerve axons being present at 60 days gestation. Nerve fibres were present in the septomarginal band at this time, however, en passant associations with ventricular Purkinje fibres were rarely observed until 140 days gestation and intimate contacts were not present at any stage. Although the AVB and ventricular Purkinje system of adult sheep are composed of morphologically similar cells, the present study demonstrates that they differ in origin and their mode of differentiation as well as timing and intimacy of innervation. Innervation is not part of the developmental mechanism leading to the differentiation of Purkinje fibres. No primordium of the ventricular Purkinje system could be identified, suggesting that the mechanism of differentiation of ventricular Purkinje fibres involves recruitment from early working myocardium.

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Takeda, Minako, Yasuo Amano, Masaki Tachi, Hitomi Tani, Kyoichi Mizuno, and Shinichiro Kumita. "MRI differentiation of cardiomyopathy showing left ventricular hypertrophy and heart failure: differentiation between cardiac amyloidosis, hypertrophic cardiomyopathy, and hypertensive heart disease." Japanese Journal of Radiology 31, no. 10 (August 31, 2013): 693–700. http://dx.doi.org/10.1007/s11604-013-0238-0.

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17

Liu, Jiabao, Peng Wu, Hao Wang, Yunle Wang, Yingqiang Du, Weili Cheng, Zhihui Xu, Ningtian Zhou, Liansheng Wang, and Zhijian Yang. "Necroptosis Induced by Ad-HGF Activates Endogenous C-Kit+ Cardiac Stem Cells and Promotes Cardiomyocyte Proliferation and Angiogenesis in the Infarcted Aged Heart." Cellular Physiology and Biochemistry 40, no. 5 (2016): 847–60. http://dx.doi.org/10.1159/000453144.

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Background/Aims: The discovery of c-kit+ cardiac stem cells (CSCs) provided us with new therapeutic targets to repair the damaged heart. However, the precise mechanisms regulating CSC proliferation and differentiation in the aged heart remained elusive. Necroptosis, a type of regulated cell death, has recently been shown to occur following myocardial infarction (MI); however, its effect on c-kit+ CSCs remains unknown. We investigated the effects of hepatocyte growth factor (HGF) and necroptosis on the proliferation and differentiation of endogenous c-kit+ CSCs in aged rat hearts following MI. Methods: The c-kit+ CSCs and HGF/p-Met expression levels in neonatal, adult and aged rats were compared using immunofluorescence and Western blotting. Immediately after MI, adenovirus carrying the HGF gene (Ad-HGF) was injected into the left ventricular wall surrounding the infarct areas of the aged rat heart. The proliferation and differentiation of the endogenous c-kit+ CSCs were studied using immunofluorescence. The signalling pathways were analysed via Western blotting and ELISA. Results: HGF/p-Met expression levels and c-kit+ CSC abundance gradually decreased with age. Ad-HGF promoted c-kit+ CSC differentiation into precursor cells of cardiomyocyte, endothelial and smooth muscle cell lineages and enhanced cardiomyocyte proliferation and angiogenesis in aged rats; these effects were reversed by the inhibition of necroptosis. Ad-HGF administration induced necroptosis by increasing the expression of receptor interacting protein kinase (RIP) 1 and receptor interacting protein kinase (RIP) 3 proteins in the infarcted heart. Moreover, Ad-HGF-induced necroptosis increased high-mobility group box 1 protein (HMGB1) levels and enhanced the abundance of c-kit+ cells in the bone marrow, which may partly account for the beneficial effect of necroptosis on the c-kit+ CSCs. Conclusion: Ad-HGF-induced necroptosis facilitated aged heart repair after MI by promoting c-kit+ CSC proliferation and differentiation. These findings may lead to the development of new methods for the treatment of ischaemic heart disease in aged populations.

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Kaarbø, Mari, Denis I. Crane, and Wayne G. Murrell. "RhoA Regulation of Cardiomyocyte Differentiation." Scientific World Journal 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/491546.

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Earlier findings from our laboratory implicated RhoA in heart developmental processes. To investigate factors that potentially regulate RhoA expression, RhoA gene organisation and promoter activity were analysed. Comparative analysis indicated strict conservation of both gene organisation and coding sequence of the chick, mouse, and human RhoA genes. Bioinformatics analysis of the derived promoter region of mouse RhoA identified putative consensus sequence binding sites for several transcription factors involved in heart formation and organogenesis generally. Using luciferase reporter assays, RhoA promoter activity was shown to increase in mouse-derived P19CL6 cells that were induced to differentiate into cardiomyocytes. Overexpression of a dominant negative mutant of mouse RhoA (mRhoAN19) blocked this cardiomyocyte differentiation of P19CL6 cells and led to the accumulation of the cardiac transcription factors SRF and GATA4 and the early cardiac marker cardiacα-actin. Taken together, these findings indicate a fundamental role for RhoA in the differentiation of cardiomyocytes.

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Fang, Yi-Hsien, Saprina P. H. Wang, Zi-Han Gao, Sheng-Nan Wu, Hsien-Yuan Chang, Pei-Jung Yang, Ping-Yen Liu, and Yen-Wen Liu. "Efficient Cardiac Differentiation of Human Amniotic Fluid-Derived Stem Cells into Induced Pluripotent Stem Cells and Their Potential Immune Privilege." International Journal of Molecular Sciences 21, no. 7 (March 29, 2020): 2359. http://dx.doi.org/10.3390/ijms21072359.

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Mature mammalian hearts possess very limited regenerative potential. The irreversible cardiomyocyte loss after heart injury can lead to heart failure and death. Pluripotent stem cells (PSCs) can differentiate into cardiomyocytes for cardiac repair, but there are obstacles to their clinical application. Among these obstacles is their potential for post-transplant rejection. Although human amniotic fluid-derived stem cells (hAFSCs) are immune privileged, they cannot induce cardiac differentiation. Thus, we generated hAFSC-derived induced PSCs (hAFSC-iPSCs) and used a Wnt-modulating differentiation protocol for the cardiac differentiation of hAFSC-iPSCs. In vitro studies using flow cytometry, immunofluorescence staining, and patch-clamp electrophysiological study, were performed to identify the characteristics of hAFSC-iPSC-derived cardiomyocytes (hAFSC-iPSC-CMs). We injected hAFSC-iPSC-CMs intramuscularly into rat infarcted hearts to evaluate the therapeutic potential of hAFSC-iPSC-CM transplantation. At day 21 of differentiation, the hAFSC-iPSC-CMs expressed cardiac-specific marker (cardiac troponin T), presented cardiomyocyte-specific electrophysiological properties, and contracted spontaneously. Importantly, these hAFSC-iPSC-CMs demonstrated low major histocompatibility complex (MHC) class I antigen expression and the absence of MHC class II antigens, indicating their low immunogenicity. The intramyocardial transplantation of hAFSC-iPSC-CMs restored cardiac function, partially remuscularized the injured region, and reduced fibrosis in the rat infarcted hearts. Therefore, hAFSC-iPSCs are potential candidates for the repair of infarcted myocardium.

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Wei, Y., D. Bader, and J. Litvin. "Identification of a novel cardiac-specific transcript critical for cardiac myocyte differentiation." Development 122, no. 9 (September 1, 1996): 2779–89. http://dx.doi.org/10.1242/dev.122.9.2779.

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A novel cDNA, pCMF1, which is expressed exclusively and transiently in the myogenic cells of the differentiating chicken heart was isolated and characterized. The full-length cDNA of pCMF1 has one open reading frame encoding 1538 predicted amino acids. While computer analysis predicts the presence of specific structural motifs, the overall sequence of pCMF1 is unique. The pattern of pCMF1 gene expression during heart formation was determined by whole-mount in situ hybridization. pCMF1 is transiently expressed within the myogenic cells of the primitive heart tube from stages 9 to 18 and is not detected in the heart or any other tissue thereafter. A replication-deficient retrovirus was used to mediate pCMF1 antisense expression in cardiogenic mesoderm. These analyses determined that the presence of pCMF1 antisense sequences disrupted myosin heavy chain expression during cardiac mesoderm differentiation. pCMF1 antisense had no effect on myosin heavy chain expression in differentiated cardiac myocytes. These data suggest a potential function for pCMF1 during cardiac myogenesis.

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Carver, W., R. L. Price, D. S. Raso, L. Terracio, and T. K. Borg. "Distribution of beta-1 integrin in the developing rat heart." Journal of Histochemistry & Cytochemistry 42, no. 2 (February 1994): 167–75. http://dx.doi.org/10.1177/42.2.8288862.

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Cell-cell and cell-matrix interactions play critical roles in various developmental processes including differentiation, proliferation, and migration. Members of the integrin family of cell surface components are important mediators of these cell-extracellular matrix (ECM) contacts or interactions. The ECM provides signals to individual cells essential for development and differentiation and plays essential roles in establishing and maintaining the complex structure of the vertebrate heart. Integrins provide a fundamental link for transduction of developmental signals to cells. Integrin expression by cardiac myocytes is altered during neonatal heart development and disease; however, little is known regarding the spatial and temporal patterns of integrin expression during embryonic and fetal heart development. Essential to understanding the role of integrins in the organization of the heart, the present studies have localized beta-1 integrin protein and mRNA in fetal and neonatal rat hearts. Beta-1 integrin is predominantly found in regions of remodeling (trabeculae) in the early heart (10-13 days of gestation). Later in development (15 days of gestation onward), beta-1 integrin is abundant in regions containing an elaborate ECM, such as the valves. These studies further support the hypothesis that the expressions of integrins and ECM are coordinately regulated in the developing heart.

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Foster, Paul S., Daniel G. Webster, and Edward W. L. Smith. "The Psychophysiological Differentiation of Emotional Memories." Imagination, Cognition and Personality 17, no. 2 (October 1997): 111–22. http://dx.doi.org/10.2190/qu7n-hqyw-86xf-wx56.

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Participants' heart rate and skin resistance responses to emotional memories (fear, anger, joy, sadness, and embarrassment) were studied to determine if the recollection of emotion is sufficient to produce psychophysiological changes, to determine if such changes differ for the various emotions, and to determine the relationship between imaginal abilities and psychophysiological responses to emotional memories. The Absorption Scale of the Multidimensional Personality Questionnaire was used as the measure of imaginal ability [1]. A repeated measures analysis of variance indicated significant differences for skin resistance but not heart rate among emotional memories, F(5,75) = 4.22, p = .002. Recollection of emotional memories, therefore, can produce psychophysiological changes in skin resistance which resemble emotions in real-life circumstances. A theoretical framework for interpretation of results on emotional memories is presented.

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Jonker, Sonnet S., Lubo Zhang, Samantha Louey, George D. Giraud, Kent L. Thornburg, and J. Job Faber. "Myocyte enlargement, differentiation, and proliferation kinetics in the fetal sheep heart." Journal of Applied Physiology 102, no. 3 (March 2007): 1130–42. http://dx.doi.org/10.1152/japplphysiol.00937.2006.

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The generation of new myocytes is an essential process of in utero heart growth. Most, or all, cardiac myocytes lose their capacity for proliferation during the perinatal period through the process of terminal differentiation. An increasing number of studies focus on how experimental interventions affect cardiac myocyte growth in the fetal sheep. Nevertheless, fundamental questions about normal growth of the fetal heart remain unanswered. In this study, we determined that during the last third of gestation the hearts of fetal sheep grew primarily by four processes. 1) Myocyte proliferation contributed substantially to daily cardiac mass gain, and the number of cardiac myocytes continued to increase to term. 2) The (hitherto unrecognized) contribution to cardiac growth by the increase in myocyte size associated with the transition from mononucleation to binucleation (terminal differentiation) became considerable from ∼115 days of gestational age (dGA) until term (145dGA). Because binucleation became the more frequent outcome of myocyte cell cycle activity after ∼115dGA, the number of binucleated myocytes increased at the expense of the number of mononucleated myocytes. Both the interval between nuclear divisions and the duration of cell cycle activity in myocytes decreased substantially during this same period. Finally, cardiac growth was in part due to enlargement of 3) mononucleated and 4) binucleated myocytes, which grew in cross-sectional diameter but not length during the last third of gestation. These data on normal cardiac growth may enable a more detailed understanding of the consequences of experimental and pathological interventions in prenatal life.

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Chen, Li, Filomena Gabriella Fulcoli, Susan Tang, and Antonio Baldini. "Tbx1 Regulates Proliferation and Differentiation of Multipotent Heart Progenitors." Circulation Research 105, no. 9 (October 23, 2009): 842–51. http://dx.doi.org/10.1161/circresaha.109.200295.

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Maisch, Bernhard, and Jörg Lauschke. "Reply to: Pitfalls in the differentiation between athlete’s heart…" Clinical Research in Cardiology 98, no. 7 (June 19, 2009): 467–68. http://dx.doi.org/10.1007/s00392-009-0036-y.

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Wollert, Kai C., and Tibor Kempf. "Growth Differentiation Factor 15 in Heart Failure: An Update." Current Heart Failure Reports 9, no. 4 (September 9, 2012): 337–45. http://dx.doi.org/10.1007/s11897-012-0113-9.

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Chang, Wei-Ting, Jhih-Yuan Shih, Yu-Wen Lin, Zhih-Cherng Chen, Jun-Neng Roan, and Chih-Hsin Hsu. "Growth differentiation factor-15 levels in the blood around the pulmonary artery is associated with hospitalization for heart failure in patients with pulmonary arterial hypertension." Pulmonary Circulation 10, no. 4 (October 2020): 204589402096294. http://dx.doi.org/10.1177/2045894020962948.

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Despite no significant differences of growth differentiation factor-15 expressions in peripheral, right atrial, and right ventricular blood, in the pulmonary arterial blood, there was a significantly high level of growth differentiation factor-15 in Group I pulmonary arterial hypertension patients subsequently developing heart failure. During right heart catheterization, collecting pulmonary blood samples is suggested to measure growth differentiation factor-15.

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Gutkowska, Jolanta, Malgorzata Miszkurka, Bogdan Danalache, Natig Gassanov, Donghao Wang, and Marek Jankowski. "Functional arginine vasopressin system in early heart maturation." American Journal of Physiology-Heart and Circulatory Physiology 293, no. 4 (October 2007): H2262—H2270. http://dx.doi.org/10.1152/ajpheart.01320.2006.

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Since the neurohypophyseal hormone 8-arginine vasopressin (AVP) is involved in cardiovascular tissue hypertrophy and myocyte differentiation, it is possible that local AVP plays a role in heart maturation. AVP-specific RIA, RT-PCR, and immunoblot measurement of AVP receptors (VR) were used to investigate heart tissues from newborn and adult rats. To test AVP's role in differentiation and specialization into ventricle-like cardiomyocytes, we studied GFP-P19Cl6 stem cells, which express green fluorescence protein (GFP) reporter under transcriptional control of the myosin light chain-2v promoter. VR1 transcripts and proteins were higher in adult than in newborn rat hearts. In contrast, VR2 increased from postnatal day 1 to 5 and was barely detected in the adult rat heart. In cardiomyocytes expressing troponin C, immunofluorescence revealed VR2 and VR1. Intracellular cAMP increased 6.5- and 8.9-fold in response to the selective VR2 agonist 1-desamino-8-d-AVP (DDAVP) after 1 and 24 h, respectively. Cardiac AVP was high in 1- and 5-day-old (330 ± 26 and 276 ± 53 pg/mg protein, respectively) but low in 66-day-old (98 ± 15 pg/mg protein) rats. AVP immunostaining was detected in the tunica adventitia and endothelium of the coronary vessels. The possible role of AVP in cardiomyogenesis was indicated by DDAVP-AVP-dependent differentiation of GFP-P19Cl6 stem cells into contracting cells displaying GATA-4, a cardiac-specific marker, and ventricle-specific myosin light chain. Together, it is suggested that the AVP system is implicated in postnatal cardiac maturation.

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Dick, H., R. G. E. Murray, and S. Walmsley. "Swarmer cell differentiation of Proteus mirabilis in fluid media." Canadian Journal of Microbiology 31, no. 11 (November 1, 1985): 1041–50. http://dx.doi.org/10.1139/m85-196.

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After 3–4 h in a rich fluid medium such as brain–heart infusion broth, motile nonseptate filaments developed from normal short rods and formed about 80% of the cell mass of Proteus mirabilis PM23. This developmental pattern was not observed in any of the other nine representatives of the species. These filaments were considered to be equivalent to swarmer cells formed on agar media because these cells ceased tumbling (i.e., chemotaxis was repressed), they developed large numbers of flagella (i.e., flagella synthesis and insertion was derepressed), and the distribution of nuclei in the filaments indicated that there was normal segregation. The population of cells grown in a minimal medium supplemented with amino acids and nicotinic acid consisted only of short cells with tumbling motility, despite the production of long cells and swarming on the same medium solidified with ordinary agar (refined agar was not effective). These short cells differentiated in 1–1.5 h in brain–heart infusion broth at 37 °C after an initial division. The requirements for initiation of differentiation were good basal nutrition, suitable cations (probably Ca2+ and Na+, or K+), and unknown heat-stable organic factors (molecular weight < 10 000) present in crude agar and yeast extract. Other components of media promoted swarmer differentiation if it was initiated and these included organic acids (lactate), amino acids (proline or serine), phosphate, and an appropriate ionic environment. Comparison of the observed sequence of length classes in brain–heart infusion broth culture with computer generated growth models suggested that, at the outset of growth, 50% of the products of each short cell division ceased septation but grew in length for about five doubling periods and then divided cells from each end at a faster rate (3–5 times per hour) for return to the short cell pool.

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Kirby, Margaret L., and Karen L. Waldo. "Molecular Embryogenesis of the Heart." Pediatric and Developmental Pathology 5, no. 6 (November 2002): 516–43. http://dx.doi.org/10.1007/s10024-002-0004-2.

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Development of the heart is a complex process involving primary and secondary heart fields that are set aside to generate myocardial and endocardial cell lineages. The molecular inductions that occur in the primary heart field appear to be recapitulated in induction and myocardial differentiation of the secondary heart field, which adds the conotruncal segments to the primary heart tube. While much is now known about the initial steps and factors involved in induction of myocardial differentiation, little is known about induction of endocardial development. Many of the genes expressed by nascent myocardial cells, which then become committed to a specific heart segment, have been identified and studied. In addition to the heart fields, several other “extracardiac” cell populations contribute to the fully functional mature heart. Less is known about the genetic programs of extracardiac cells as they enter the heart and take part in cardiogenesis. The molecular/genetic basis of many congenital cardiac defects has been elucidated in recent years as a result of new insights into the molecular control of developmental events.

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Yong, Hue Mun Au, Erica Minato, Eldho Paul, and Udaya Seneviratne. "006 Can seizure-related heart rate differentiate epileptic seizures from psychogenic non-epileptic seizures?" Journal of Neurology, Neurosurgery & Psychiatry 90, e7 (July 2019): A2.3—A3. http://dx.doi.org/10.1136/jnnp-2019-anzan.6.

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IntroductionThis study aims to (i)evaluate the diagnostic sensitivity, specificity and predictive values of seizure-related heart rate (HR) in differentiating epileptic seizures(ES) from psychogenic non-epileptic seizures(PNES), (ii)define the most useful point of HR measurement: pre-ictal, ictal-onset, maximal-ictal or post-ictal, and (iii)define the HR cut-off points to differentiate ES from PNES.MethodsAll video EEG(VEEG) at Monash Health from May 2009 to November 2015 were retrospectively reviewed. Baseline(during wakefulness), one-minute pre-ictal, ictal-onset, maximal-ictal and one-minute post-ictal HR were measured for each ES and PNES event. Events less than ten seconds or with uninterpretable ECG due to artefacts were excluded. ROC curve analysis was performed to study the diagnostic accuracy reflected by area under the curve(AUC). The AUC was interpreted as follows; ≤0.5, differentiation of PNES from ES no better than chance; 0.80–0.89, good differentiation; and 0.9–1, excellent differentiation.ResultsVEEG of 341 ES and 265 PNES from 130 patients were analysed. The AUC for pre-ictal, ictal-onset, maximal-ictal and post-ictal HR were found to have poor differentiation between ES and PNES. Comparing PNES and bilateral tonic-clonic ES, AUC for absolute maximal-ictal HR was 0.84(CI 0.73–0.95) and for absolute post-ictal HR was 0.90(CI 0.81–1.00). Using Youden’s index, to diagnose tonic-clonic ES, the optimal cut-off point for absolute maximal-ictal HR was 114bpm (sensitivity 84%;specificity 82%;PPV 26.7%,NPV 98.5%) and for absolute post-ictal HR was 90bpm(sensitivity 91%;specificity 82%;PPV 30.3%;NPV 99.1%).ConclusionsThese findings suggest that seizure-related HR increase is useful in differentiating bilateral tonic-clonic ES from PNES. Based on the AUC, the best diagnostic measureme.

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Bondue, Antoine, Simon Tännler, Giuseppe Chiapparo, Samira Chabab, Mirana Ramialison, Catherine Paulissen, Benjamin Beck, Richard Harvey, and Cédric Blanpain. "Defining the earliest step of cardiovascular progenitor specification during embryonic stem cell differentiation." Journal of Cell Biology 192, no. 5 (March 7, 2011): 751–65. http://dx.doi.org/10.1083/jcb.201007063.

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During embryonic development and embryonic stem cell (ESC) differentiation, the different cell lineages of the mature heart arise from two types of multipotent cardiovascular progenitors (MCPs), the first and second heart fields. A key question is whether these two MCP populations arise from differentiation of a common progenitor. In this paper, we engineered Mesp1–green fluorescent protein (GFP) ESCs to isolate early MCPs during ESC differentiation. Mesp1-GFP cells are strongly enriched for MCPs, presenting the ability to differentiate into multiple cardiovascular lineages from both heart fields in vitro and in vivo. Transcriptional profiling of Mesp1-GFP cells uncovered cell surface markers expressed by MCPs allowing their prospective isolation. Mesp1 is required for MCP specification and the expression of key cardiovascular transcription factors. Isl1 is expressed in a subset of early Mesp1-expressing cells independently of Mesp1 and acts together with Mesp1 to promote cardiovascular differentiation. Our study identifies the early MCPs residing at the top of the cellular hierarchy of cardiovascular lineages during ESC differentiation.

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Behfar, Atta, Carmen Perez-Terzic, Randolph S. Faustino, D. Kent Arrell, Denice M. Hodgson, Satsuki Yamada, Michel Puceat, et al. "Cardiopoietic programming of embryonic stem cells for tumor-free heart repair." Journal of Experimental Medicine 204, no. 2 (February 5, 2007): 405–20. http://dx.doi.org/10.1084/jem.20061916.

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Embryonic stem cells have the distinct potential for tissue regeneration, including cardiac repair. Their propensity for multilineage differentiation carries, however, the liability of neoplastic growth, impeding therapeutic application. Here, the tumorigenic threat associated with embryonic stem cell transplantation was suppressed by cardiac-restricted transgenic expression of the reprogramming cytokine TNF-α, enhancing the cardiogenic competence of recipient heart. The in vivo aptitude of TNF-α to promote cardiac differentiation was recapitulated in embryoid bodies in vitro. The procardiogenic action required an intact endoderm and was mediated by secreted cardio-inductive signals. Resolved TNF-α–induced endoderm-derived factors, combined in a cocktail, secured guided differentiation of embryonic stem cells in monolayers produce cardiac progenitors termed cardiopoietic cells. Characterized by a down-regulation of oncogenic markers, up-regulation, and nuclear translocation of cardiac transcription factors, this predetermined population yielded functional cardiomyocyte progeny. Recruited cardiopoietic cells delivered in infarcted hearts generated cardiomyocytes that proliferated into scar tissue, integrating with host myocardium for tumor-free repair. Thus, cardiopoietic programming establishes a strategy to hone stem cell pluripotency, offering a tumor-resistant approach for regeneration.

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Jackson, T., M. F. Allard, C. M. Sreenan, L. K. Doss, S. P. Bishop, and J. L. Swain. "The c-myc proto-oncogene regulates cardiac development in transgenic mice." Molecular and Cellular Biology 10, no. 7 (July 1990): 3709–16. http://dx.doi.org/10.1128/mcb.10.7.3709.

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During the maturation of the cardiac myocyte, a transition occurs from hyperplastic to hypertrophic growth. The factors that control this transition in the developing heart are unknown. Proto-oncogenes such as c-myc have been implicated in the regulation of cellular proliferation and differentiation, and in the heart the switch from myocyte proliferation to terminal differentiation is synchronous with a decrease in c-myc mRNA abundance. To determine whether c-myc can influence myocyte proliferation or differentiation, we examined the in vivo effect of increasing c-myc expression during embryogenesis and of preventing the decrease in c-myc mRNA expression that normally occurs during cardiac development. The model system used was a strain of transgenic mice exhibiting constitutive expression of c-myc mRNA in cardiac myocytes throughout development. In these transgenic mice, increased c-myc mRNA expression was found to be associated with both atrial and ventricular enlargement. This increase in cardiac mass was secondary to myocyte hyperplasia, with the transgenic hearts containing more than twice as many myocytes as did nontransgenic hearts. The results suggest that in the transgenic animals there is additional hyperplastic growth during fetal development. However, this additional proliferative growth is not reflected in abnormal myocyte maturation, as assessed by the expression of the cardiac and skeletal isoforms of alpha-actin. The results of this study indicate that constitutive expression of c-myc mRNA in the heart during development results in enhanced hyperplastic growth and suggest a regulatory role for this proto-oncogene in cardiac myogenesis.

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Jackson, T., M. F. Allard, C. M. Sreenan, L. K. Doss, S. P. Bishop, and J. L. Swain. "The c-myc proto-oncogene regulates cardiac development in transgenic mice." Molecular and Cellular Biology 10, no. 7 (July 1990): 3709–16. http://dx.doi.org/10.1128/mcb.10.7.3709-3716.1990.

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During the maturation of the cardiac myocyte, a transition occurs from hyperplastic to hypertrophic growth. The factors that control this transition in the developing heart are unknown. Proto-oncogenes such as c-myc have been implicated in the regulation of cellular proliferation and differentiation, and in the heart the switch from myocyte proliferation to terminal differentiation is synchronous with a decrease in c-myc mRNA abundance. To determine whether c-myc can influence myocyte proliferation or differentiation, we examined the in vivo effect of increasing c-myc expression during embryogenesis and of preventing the decrease in c-myc mRNA expression that normally occurs during cardiac development. The model system used was a strain of transgenic mice exhibiting constitutive expression of c-myc mRNA in cardiac myocytes throughout development. In these transgenic mice, increased c-myc mRNA expression was found to be associated with both atrial and ventricular enlargement. This increase in cardiac mass was secondary to myocyte hyperplasia, with the transgenic hearts containing more than twice as many myocytes as did nontransgenic hearts. The results suggest that in the transgenic animals there is additional hyperplastic growth during fetal development. However, this additional proliferative growth is not reflected in abnormal myocyte maturation, as assessed by the expression of the cardiac and skeletal isoforms of alpha-actin. The results of this study indicate that constitutive expression of c-myc mRNA in the heart during development results in enhanced hyperplastic growth and suggest a regulatory role for this proto-oncogene in cardiac myogenesis.

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Wu, Mingfu, and Jingjing Li. "Numb family proteins: novel players in cardiac morphogenesis and cardiac progenitor cell differentiation." Biomolecular Concepts 6, no. 2 (April 1, 2015): 137–48. http://dx.doi.org/10.1515/bmc-2015-0003.

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AbstractVertebrate heart formation is a spatiotemporally regulated morphogenic process that initiates with bilaterally symmetric cardiac primordial cells migrating toward the midline to form a linear heart tube. The heart tube then elongates and undergoes a series of looping morphogenesis, followed by expansions of regions that are destined to become primitive heart chambers. During the cardiac morphogenesis, cells derived from the first heart field contribute to the primary heart tube, and cells from the secondary heart field, cardiac neural crest, and pro-epicardial organ are added to the heart tube in a precise spatiotemporal manner. The coordinated addition of these cells and the accompanying endocardial cushion morphogenesis yield the atrial, ventricular, and valvular septa, resulting in the formation of a four-chambered heart. Perturbation of progenitor cells’ deployment and differentiation leads to a spectrum of congenital heart diseases. Two of the genes that were recently discovered to be involved in cardiac morphogenesis are Numb and Numblike. Numb, an intracellular adaptor protein, distinguishes sibling cell fates by its asymmetric distribution between the two daughter cells and its ability to inhibit Notch signaling. Numb regulates cardiac progenitor cell differentiation in Drosophila and controls heart tube laterality in Zebrafish. In mice, Numb and Numblike, the Numb family proteins (NFPs), function redundantly and have been shown to be essential for epicardial development, cardiac progenitor cell differentiation, outflow tract alignment, atrioventricular septum morphogenesis, myocardial trabeculation, and compaction. In this review, we will summarize the functions of NFPs in cardiac development and discuss potential mechanisms of NFPs in the regulation of cardiac development.

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Hamid, Tariq, Yuanyuan Xu, Mohamed Ameen Ismahil, Qianhong Li, Steven P. Jones, Aruni Bhatnagar, Roberto Bolli, and Sumanth D. Prabhu. "TNF receptor signaling inhibits cardiomyogenic differentiation of cardiac stem cells and promotes a neuroadrenergic-like fate." American Journal of Physiology-Heart and Circulatory Physiology 311, no. 5 (November 1, 2016): H1189—H1201. http://dx.doi.org/10.1152/ajpheart.00904.2015.

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Despite expansion of resident cardiac stem cells (CSCs; c-kit+Lin−) after myocardial infarction, endogenous repair processes are insufficient to prevent adverse cardiac remodeling and heart failure (HF). This suggests that the microenvironment in post-ischemic and failing hearts compromises CSC regenerative potential. Inflammatory cytokines, such as tumor necrosis factor-α (TNF), are increased after infarction and in HF; whether they modulate CSC function is unknown. As the effects of TNF are specific to its two receptors (TNFRs), we tested the hypothesis that TNF differentially modulates CSC function in a TNFR-specific manner. CSCs were isolated from wild-type (WT), TNFR1−/−, and TNFR2−/− adult mouse hearts, expanded and evaluated for cell competence and differentiation in vitro in the absence and presence of TNF. Our results indicate that TNF signaling in murine CSCs is constitutively related primarily to TNFR1, with TNFR2 inducible after stress. TNFR1 signaling modestly diminished CSC proliferation, but, along with TNFR2, augmented CSC resistance to oxidant stress. Deficiency of either TNFR1 or TNFR2 did not impact CSC telomerase activity. Importantly, TNF, primarily via TNFR1, inhibited cardiomyogenic commitment during CSC differentiation, and instead promoted smooth muscle and endothelial fates. Moreover, TNF, via both TNFR1 and TNFR2, channeled an alternate CSC neuroadrenergic-like fate (capable of catecholamine synthesis) during differentiation. Our results suggest that elevated TNF in the heart restrains cardiomyocyte differentiation of resident CSCs and may enhance adrenergic activation, both effects that would reduce the effectiveness of endogenous cardiac repair and the response to exogenous stem cell therapy, while promoting adverse cardiac remodeling. Listen to this article's corresponding podcast at http://ajpheart.podbean.com/e/tnf-and-cardiac-stem-cell-differentiation/ .

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Bogdanov, L. A., and A. G. Kutikhin. "Optimization of hematoxylin and eosin staining of heart, blood vessels, liver, and spleen." Fundamental and Clinical Medicine 4, no. 4 (December 28, 2019): 70–77. http://dx.doi.org/10.23946/2500-0764-2019-4-4-70-77.

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Aim. To optimize hematoxylin and eosin staining protocol for heart, blood vessels, liver, and spleen.Methods. Heart (ventricles), abdominal aorta, liver (right lobe), and spleen (left part) of the Wistar rats were excised, fixed in 10% neutral phosphate buffered formalin for 24 h, washed in tap water for 2 h, dehydrated in ascending ethanol series (70%, 80%, and 95%) and isopropanol, embedded into paraffin and then sectioned (5 μm) using rotary microtome. For regressive staining, incubation time in Harris hematoxylin was 5 or 10 minutes, time of exposure to differentiation alcoholicaqueous eosin was 1 or 2 minutes. For progressive staining, incubation time in Carazzi’s hematoxylin and eosin was the same but the differentiation solution was not utilized.Results. Progressive staining retained tissue integrity and accelerated staining protocol as compared to regressive staining due to absence of exposure to aggressive acid alcohol differentiation solution. The optimized protocol for heart, aorta and liver, similar for regressive and progressive staining, included incubation in hematoxylin for 10 minutes and eosin for 2 minutes. Time of exposure to differentiation solution (2 or 10 seconds) was defined by the desirable shade. For spleen, however, the optimized protocol included staining in hematoxylin for 5 minutes and eosin for 2 minutes, with 10 seconds in differentiation solution for regressive staining.Conclusion. Progressive hematoxylin is preferable over regressive hematoxylin for staining of heart, aorta, liver, and spleen.

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Urhausen, Axel, and Wilfried Kindermann. "Sports-Specific Adaptations and Differentiation of the Athlete??s Heart." Sports Medicine 28, no. 4 (1999): 237–44. http://dx.doi.org/10.2165/00007256-199928040-00002.

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Lim, Jeong A., Hye Jung Baek, Moon Sun Jang, Eun Kyoung Choi, Yong Min Lee, Sang Jin Lee, Sung Chul Lim, et al. "Loss of β2-spectrin prevents cardiomyocyte differentiation and heart development." Cardiovascular Research 101, no. 1 (September 24, 2013): 39–47. http://dx.doi.org/10.1093/cvr/cvt222.

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Calderon, Damelys, Evan Bardot, and Nicole Dubois. "Probing early heart development to instruct stem cell differentiation strategies." Developmental Dynamics 245, no. 12 (October 3, 2016): 1130–44. http://dx.doi.org/10.1002/dvdy.24441.

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Sapoznikov, Dan, Myron H. Luria, and Mervyn S. Gotsman. "Differentiation of Periodic from Nonperiodic Low-Frequency Heart Rate Fluctuations." Computers and Biomedical Research 27, no. 3 (June 1994): 199–209. http://dx.doi.org/10.1006/cbmr.1994.1017.

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Anand, Inder S., Tibor Kempf, Thomas S. Rector, Heike Tapken, Tim Allhoff, Franziska Jantzen, Michael Kuskowski, Jay N. Cohn, Helmut Drexler, and Kai C. Wollert. "Serial Measurement of Growth-Differentiation Factor-15 in Heart Failure." Circulation 122, no. 14 (October 5, 2010): 1387–95. http://dx.doi.org/10.1161/circulationaha.109.928846.

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Risebro, C. A., N. Smart, L. Dupays, R. Breckenridge, T. J. Mohun, and P. R. Riley. "Hand1 regulates cardiomyocyte proliferation versus differentiation in the developing heart." Development 133, no. 22 (October 11, 2006): 4595–606. http://dx.doi.org/10.1242/dev.02625.

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Millar, Lynne Martina, Zephryn Fanton, Gherardo Finocchiaro, Gabriel Sanchez-Fernandez, Harshil Dhutia, Aneil Malhotra, Ahmed Merghani, et al. "Differentiation between athlete’s heart and dilated cardiomyopathy in athletic individuals." Heart 106, no. 14 (April 27, 2020): 1059–65. http://dx.doi.org/10.1136/heartjnl-2019-316147.

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ObjectiveDistinguishing early dilated cardiomyopathy (DCM) from physiological left ventricular (LV) dilatation with LV ejection fraction <55% in athletes (grey zone) is challenging. We evaluated the role of a cascade of investigations to differentiate these two entities.MethodsThirty-five asymptomatic active males with DCM, 25 male athletes in the ‘grey zone’ and 24 male athletes with normal LV ejection fraction underwent N-terminal pro-brain natriuretic peptide (NT-proBNP) measurement, ECG and exercise echocardiography. Grey-zone athletes and patients with DCM underwent cardiovascular magnetic resonance (CMR) and Holter monitoring.ResultsLarger LV cavity dimensions and lower LV ejection fraction were the only differences between grey-zone and control athletes. None of the grey-zone athletes had abnormal NT-proBNP, increased ectopic burden/complex arrhythmias or pathological late gadolinium enhancement on CMR. These features were also absent in 71%, 71% and 50% of patients with DCM, respectively. 95% of grey-zone athletes and 60% of patients with DCM had normal ECG. During exercise echocardiography, 96% grey-zone athletes increased LV ejection fraction by >11% from baseline to peak exercise compared with 23% of patients with DCM (p<0.0001). Peak LV ejection fraction was >63% in 92% grey-zone athletes compared with 17% patients with DCM (p<0.0001). Failure to increase LV ejection fraction >11% from baseline to peak exercise or achieve a peak LV ejection fraction >63% had sensitivity of 77% and 83%, respectively, and specificity of 96% and 92%, respectively, for predicting DCM.ConclusionComprehensive assessment using a cascade of routine investigations revealed that exercise stress echocardiography has the greatest discriminatory value in differentiating between grey-zone athletes and asymptomatic patients with DCM. Our findings require validation in larger studies.

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Behfar, Atta, Leonid V. Zingman, Denice M. Hodgson, Jean‐Michel Rauzier, Garvan C. Kane, Andre Terzic, and Michel Pucéat. "Stem cell differentiation requires a paracrine pathway in the heart." FASEB Journal 16, no. 12 (October 2002): 1558–66. http://dx.doi.org/10.1096/fj.02-0072com.

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Breckwoldt, Kaja, David Letuffe-Brenière, Ingra Mannhardt, Thomas Schulze, Bärbel Ulmer, Tessa Werner, Anika Benzin, et al. "Differentiation of cardiomyocytes and generation of human engineered heart tissue." Nature Protocols 12, no. 6 (May 11, 2017): 1177–97. http://dx.doi.org/10.1038/nprot.2017.033.

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Scharhag, Jürgen, and Wilfried Kindermann. "Pitfalls in the differentiation between athlete’s heart and hypertrophic cardiomyopathy." Clinical Research in Cardiology 98, no. 7 (June 11, 2009): 465–66. http://dx.doi.org/10.1007/s00392-009-0035-z.

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Lourenço, Patrícia, Filipe M. Cunha, João Ferreira‐Coimbra, Isaac Barroso, João‐Tiago Guimarães, and Paulo Bettencourt. "Dynamics of growth differentiation factor 15 in acute heart failure." ESC Heart Failure 8, no. 4 (May 2, 2021): 2527–34. http://dx.doi.org/10.1002/ehf2.13377.

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Rajala, Kristiina, Mari Pekkanen-Mattila, and Katriina Aalto-Setälä. "Cardiac Differentiation of Pluripotent Stem Cells." Stem Cells International 2011 (2011): 1–12. http://dx.doi.org/10.4061/2011/383709.

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The ability of human pluripotent stem cells to differentiate towards the cardiac lineage has attracted significant interest, initially with a strong focus on regenerative medicine. The ultimate goal to repair the heart by cardiomyocyte replacement has, however, proven challenging. Human cardiac differentiation has been difficult to control, but methods are improving, and the process, to a certain extent, can be manipulated and directed. The stem cell-derived cardiomyocytes described to date exhibit rather immature functional and structural characteristics compared to adult cardiomyocytes. Thus, a future challenge will be to develop strategies to reach a higher degree of cardiomyocyte maturationin vitro, to isolate cardiomyocytes from the heterogeneous pool of differentiating cells, as well as to guide the differentiation into the desired subtype, that is, ventricular, atrial, and pacemaker cells. In this paper, we will discuss the strategies for the generation of cardiomyocytes from pluripotent stem cells and their characteristics, as well as highlight some applications for the cells.

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Journal articles on the topic 'Heart – Differentiation'

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