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  • 1
    Online Resource
    Online Resource
    Differentiation Pathways in Human Embryonic Stem Cell‐Derived Cardiomyocytes
    Wiley ; 2005
    In:  Annals of the New York Academy of Sciences Vol. 1047, No. 1 ( 2005-06), p. 50-65
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1047, No. 1 ( 2005-06), p. 50-65
    Abstract: A bstract : Human embryonic stem (hES) cells are pluripotent cell lines derived from the inner cell mass of the blastocyst‐stage embryo. These unique cell lines can be propagated in the undifferentiated state in culture, while retaining the capacity to differentiate into derivatives of all three germ layers, including cardiomyocytes. The derivation of the hES cell lines presents a powerful tool to explore the early events of cardiac progenitor cell specification and differentiation, and it also provides a novel cell source for the emerging field of cardiovascular regenerative medicine. A spontaneous differentiation system of these stem cells to cardiomyocytes was established and the generated myocytes displayed molecular, structural, and functional properties of early‐stage heart cells. In order to follow the in vitro differentiation process, the temporal expression of signaling molecules and transcription factors governing early cardiac differentiation was examined throughout the process. A characteristic pattern was noted recapitulating the normal in vivo cardiac differentiation scheme observed in other model systems. This review discusses the known pathways involved in cardiac specification and the possible factors that may be used to enhance cardiac differentiation of hES cells, as well as the steps required to fully harness the enormous potential of these unique cells.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1341.005
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2005
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  • 2
    Online Resource
    Online Resource
    Mechanism of spontaneous excitability in human embryonic stem cell derived cardiomyocytes
    Wiley ; 2004
    In:  The Journal of Physiology Vol. 559, No. 2 ( 2004-09), p. 479-496
    Details
    In: The Journal of Physiology, Wiley, Vol. 559, No. 2 ( 2004-09), p. 479-496
    Abstract: Human embryonic stem cell‐derived cardiomyocytes (hES‐CMs) are thought to recapitulate the embryonic development of heart cells. Given the exciting potential of hES‐CMs as replacement tissue in diseased hearts, we investigated the pharmacological sensitivity and ionic current of mid‐stage hES‐CMs (20–35 days post plating). A high‐resolution microelectrode array was used to assess conduction in multicellular preparations of hES‐CMs in spontaneously contracting embryoid bodies (EBs). TTX (10 μ m ) dramatically slowed conduction velocity from 5.1 to 3.2 cm s −1 while 100 μ m TTX caused complete cessation of spontaneous electrical activity in all EBs studied. In contrast, the Ca 2+ channel blockers nifedipine or diltiazem (1 μ m ) had a negligible effect on conduction. These results suggested a prominent Na + channel current, and therefore we patch‐clamped isolated cells to record Na + current and action potentials (APs). We found for isolated hES‐CMs a prominent Na + current (244 ± 42 pA pF −1 at 0 mV; n = 19), and a hyperpolarization‐activated current (HCN), but no inward rectifier K + current. In cell clusters, 3 μ m TTX induced longer AP interpulse intervals and 10 μ m TTX caused cessation of spontaneous APs. In contrast nifedipine (Ca 2+ channel block) and 2 m m Cs + (HCN complete block) induced shorter AP interpulse intervals. In single cells, APs stimulated by current pulses had a maximum upstroke velocity (d V /d t max ) of 118 ± 14 V s −1 in control conditions; in contrast, partial block of Na + current significantly reduced stimulated d V /d t max (38 ± 15 V s −1 ). RT‐PCR revealed Na V 1.5, Ca V 1.2, and HCN‐2 expression but we could not detect Kir2.1. We conclude that hES‐CMs at mid‐range development express prominent Na + current. The absence of background K + current creates conditions for spontaneous activity that is sensitive to TTX in the same range of partial block of Na V 1.5; thus, the Na V 1.5 Na + channel is important for initiating spontaneous excitability in hES‐derived heart cells.
    Type of Medium: Online Resource
    ISSN: 0022-3751 , 1469-7793
    URL: Article
    DOI: 10.1113/jphysiol.2004.068213
    RVK:
    WA 15000
    Language: English
    Publisher: Wiley
    Publication Date: 2004
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    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Extracellular signal‐regulated kinase 1/2 (ERK1/2) signaling in cardiac hypertrophy
    Wiley ; 2010
    In:  Annals of the New York Academy of Sciences Vol. 1188, No. 1 ( 2010-02), p. 96-102
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1188, No. 1 ( 2010-02), p. 96-102
    Abstract: Cardiac hypertrophy results from increased mechanical load on the heart and through the action of neurohumoral mediators. ERK1/2 are known to be activated in response to almost every stress‐ and agonist‐induced hypertrophic stimulus examined to date, suggesting the straightforward hypothesis that these kinases are required for promoting the cardiac growth response. However, recent data from genetically modified mouse models suggest a more complicated picture. For example, inducible expression of dual‐specificity phosphatase 6, an ERK1/2‐inactivating phosphatase, eliminated ERK1/2 phosphorylation in transgenic mice, but it did not diminish the hypertrophic response to pressure overload. Similarly, Erk1 −/− and Erk2 +/− mice showed no reduction in stimulus‐induced cardiac growth in vivo . However, blockade or deletion of cardiac ERK1/2 did predispose the heart to decompensation and failure after long‐term pressure overload. Thus, ERK1/2 signaling is not to be absolutely necessary for mediating cardiac hypertrophy, although it does appear to provide critical protective effects/signals during stress‐stimulation.
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Issue
    URL: Article
    DOI: 10.1111/nyas.2010.1188.issue-1
    DOI: 10.1111/j.1749-6632.2009.05088.x
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2010
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    SSG: 11
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  • 4
    Online Resource
    Online Resource
    The Role of Basic Leucine Zipper Protein‐Mediated Transcription in Physiological and Pathological Myocardial Hypertrophy
    Wiley ; 2006
    In:  Annals of the New York Academy of Sciences Vol. 1080, No. 1 ( 2006-10), p. 97-109
    Details
    In: Annals of the New York Academy of Sciences, Wiley, Vol. 1080, No. 1 ( 2006-10), p. 97-109
    Abstract: Abstract:  Accumulating evidence suggests that nuclear transcription factors from the basic leucine zipper (bZIP) family play an important role in cardiac development and function. This class includes the CREB/ATF family of transcription factors, namely CREB, cAMP response element modulator (CREM), ATF, and the related AP‐1 and C/EBP families. An effort has been made to elucidate the role of specific bZIP members in the heart. Unfortunately, little insight could be gained from knockout experiments, either due to embryonic lethal phenotypes or functional compensation by other bZIP family members. Surprisingly, cardiac overexpression of several inhibitory transcription factors from the bZIP family, such as a nonphosphorylatable form of CREB (CREB ser133 ), a nonfunctional isoform of CREM, or ATF3 resulted in massive atrial dilatation. In order to try and characterize this pathway we have expressed the potent bZIP inhibitory protein, Jun dimerization protein 2 (JDP2), specifically in the mouse heart in a temporally controlled manner. Expression of JDP2 resulted in massive biatrial dilatation; loss of connexin 40 (Cx40), connexin43 (C×43), and myosin light chain 2 (MLC2a) expression; atrioventricular defects in conduction; and a lethal phenotype. All these effects were independent of any developmental events acquired during adulthood, and were totally reversible upon abolishing the bZIP inhibition. The results of this article suggest that bZIP inhibition is sufficient to cause atrial dilation, that this dilatation is acquired postnatally, and that it is reversible upon the relief of inhibition. Thus, bZIP repressors may serve as novel drug targets for the prevention of atrial dilatation a major risk of atrial fibrillation (AF).
    Type of Medium: Online Resource
    ISSN: 0077-8923 , 1749-6632
    URL: Article
    DOI: 10.1196/annals.1380.009
    RVK:
    TD 7650
    Language: English
    Publisher: Wiley
    Publication Date: 2006
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  • 5
    Online Resource
    Online Resource
    Identification and selection of cardiomyocytes during human embryonic stem cell differentiation
    Wiley ; 2007
    In:  The FASEB Journal Vol. 21, No. 10 ( 2007-08), p. 2551-2563
    Details
    In: The FASEB Journal, Wiley, Vol. 21, No. 10 ( 2007-08), p. 2551-2563
    Type of Medium: Online Resource
    ISSN: 0892-6638 , 1530-6860
    URL: Issue
    URL: Article
    DOI: 10.1096/fsb2.v21.10
    DOI: 10.1096/fj.05-5711com
    Language: English
    Publisher: Wiley
    Publication Date: 2007
    detail.hit.zdb_id: 1468876-1
    SSG: 12
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