ORCID Profile
0000-0001-7558-8601
Current Organisations
Columbia University Medical Center
,
University of Oxford
,
University of Cambridge
,
Tufts University School of Medicine
Does something not look right? The information on this page has been harvested from data sources that may not be up to date. We continue to work with information providers to improve coverage and quality. To report an issue, use the Feedback Form.
Publisher: Elsevier BV
Date: 2009
DOI: 10.1016/S1472-6483(10)60270-2
Abstract: Human embryonic stem cells (hESC) hold great promise for use in regenerative medicine. However, the extraordinary potential of hESC as therapeutic tools is tempered by ethical, moral and political issues surrounding their derivation from human embryos. It has previously been proposed that ethical criteria applied to essential organ donation could be employed for derivation of hESC from irreversibly arrested, and thus organismically dead, human embryos produced during routine IVF procedures. Here, it is shown that arrested embryos do not resume normal development during extended culture, yet most of them contain a substantial number of living cells on embryonic day 6 (72% have <1 viable cell, 47% have <5 viable cells), suggesting that this class of non-viable embryos could be a rich source of viable cells for derivation of hESC lines.
Publisher: Ovid Technologies (Wolters Kluwer Health)
Date: 16-02-2007
DOI: 10.1161/01.RES.0000258019.74591.B3
Abstract: The sinoatrial node, which resides at the junction of the right atrium and the superior caval vein, contains specialized myocardial cells that initiate the heart beat. Despite this fundamental role in heart function, the embryonic origin and mechanisms of localized formation of the sinoatrial node have not been defined. Here we show that subsequent to the formation of the Nkx2-5 –positive heart tube, cells bordering the inflow tract of the heart tube give rise to the Nkx2-5 –negative myocardial cells of the sinoatrial node and the sinus horns. Using genetic models, we show that as the myocardium of the heart tube matures, Nkx2-5 suppresses pacemaker channel gene Hcn4 and T-box transcription factor gene Tbx3 , thereby enforcing a progressive confinement of their expression to the forming Nkx2-5 –negative sinoatrial node and sinus horns. Thus, Nkx2-5 is essential for establishing a gene expression border between the atrium and sinoatrial node. Tbx3 was found to suppress chamber differentiation, providing an additional mechanism by which the Tbx3 -positive sinoatrial node is shielded from differentiating into atrial myocardium. Pitx2c -deficient fetuses form sinoatrial nodes with indistinguishable molecular signatures at both the right and left sinuatrial junction, indicating that Pitx2c functions within the left/right pathway to suppress a default program for sinuatrial node formation on the left. Our molecular pathway provides a mechanism for how pacemaker activity becomes progressively relegated to the most recently added components of the venous pole of the heart and, ultimately, to the junction of the right atrium and superior caval vein.
Publisher: Wiley
Date: 12-10-2010
DOI: 10.1002/DVDY.22449
Publisher: Public Library of Science (PLoS)
Date: 25-07-2013
Publisher: The Company of Biologists
Date: 02-2005
DOI: 10.1242/JCS.01666
Abstract: Generation of inside cells that develop into inner cell mass (ICM) and outside cells that develop into trophectoderm is central to the development of the early mouse embryo. Critical to this decision is the development of cell polarity and the associated asymmetric (differentiative) isions of the 8-cell-stage blastomeres. The underlying molecular mechanisms for these events are not understood. As the Par3/aPKC complex has a role in establishing cellular polarity and ision orientation in other systems, we explored its potential function in the developing mouse embryo. We show that both Par3 and aPKC adopt a polarized localization from the 8-cell stage onwards and that manipulating their function re-directs cell positioning and consequently influences cell fate. Injection of dsRNA against Par3 or mRNA for a dominant negative form of aPKC into a random blastomere at the 4-cell stage directs progeny of the injected cell into the inside part of the embryo. This appears to result from both an increased frequency by which such cells undertake differentiative isions and their decreased probability of retaining outside positions. Thus, the natural spatial allocation of blastomere progeny can be over-ridden by downregulation of Par3 or aPKC, leading to a deceased tendency for them to remain outside and so develop into trophectoderm. In addition, this experimental approach illustrates a powerful means of manipulating gene expression in a specific clonal population of cells in the preimplantation embryo.
Location: United States of America
Location: United Kingdom of Great Britain and Northern Ireland
Location: United Kingdom of Great Britain and Northern Ireland
Location: United States of America
No related grants have been discovered for Virginia Papaioannou.