Abstract：
:Epithelial-mesenchymal transition is implicated in the remodelling of tissues during development and in the adult life. In the heart, it gives origin to progenitors of fibroblasts, coronary endothelium, smooth muscle cells, and cardiomyocytes. Moreover, epicardially-derived cells determine myocardial wall thickness and Purkinje fibre network. Recently, the presence of numerous cardiac stem cells in the subepicardium of the adult human heart has been described and the hypothesis that epicardially-derived cells can contribute to the population of cardiac stem cells in the adult heart has been advanced. In an effort to test this hypothesis and establish a possible link between epicardium, epicardially-derived cells and cardiac stem cells in the adult human heart we have examined epicardial mesothelial cells in the normal and pathological adult human heart with ischemic cardiomyopathy in vivo and we have induced and documented their epithelial-mesenchymal transition in vitro. Noticeably, epicardial cells were missing from the surface of pathological hearts and the cells with the expression of epithelial and mesenchymal markers populated thick subepicardial space. When the fragments of epicardium from the normal hearts were cultured on the specific substrate formed by extracellular matrix derived from cardiac fibroblasts, we obtained the outgrowth of the epithelial sheet with the mRNA and protein expression characteristic of epicardium. TGFβ induced cellular and molecular changes typical of epithelial-mesenchymal transition. Moreover, the epicardially-derived cells expressed CD117 antigen. Thus, this study provides evidence that cardiac stem cells can originate from epithelial-mesenchymal transition of the epicardial cells in the adult human heart.
journal_name
J Mol Cell Cardioljournal_title
Journal of molecular and cellular cardiologyauthors
Di Meglio F,Castaldo C,Nurzynska D,Romano V,Miraglia R,Bancone C,Langella G,Vosa C,Montagnani Sdoi
10.1016/j.yjmcc.2010.05.013subject
Has Abstractpub_date
2010-11-01 00:00:00pages
719-27issue
5eissn
0022-2828issn
1095-8584pii
S0022-2828(10)00232-4journal_volume
49pub_type
杂志文章abstract：:Cardiac alpha(1)-adrenoceptors (AR) have two predominant subtypes (alpha(1A)-AR and alpha(1B)-AR) however, their roles in regulating contraction are unclear. We determined the effects of stimulating alpha(1A)-AR (using the subtype-selective agonist A61603) and alpha(1B)-AR (using a gene knockout mouse lacking alpha(1A...
journal_title：Journal of molecular and cellular cardiology
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journal_title：Journal of molecular and cellular cardiology
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journal_title：Journal of molecular and cellular cardiology
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
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更新日期：2008-01-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章,评审
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
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更新日期：2013-12-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2015.12.008
更新日期：2016-01-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2006.03.426
更新日期：2006-07-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/0022-2828(95)90090-x
更新日期：1995-02-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2007.06.013
更新日期：2007-09-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章,评审
doi：10.1006/jmcc.2002.2066
更新日期：2002-09-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章,评审
doi：10.1016/j.yjmcc.2015.02.013
更新日期：2015-05-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章,评审
doi：10.1016/j.yjmcc.2013.12.015
更新日期：2014-06-01 00:00:00
abstract：:ADP-ribosylation factors (ARFs) are approximately 20-kDa, guanine nucleotide-binding proteins, initially discovered as stimulators of cholera toxin ADP-ribosyltransferase activity and subsequently shown to participate in vesicular trafficking. Five of the six mammalian ARFs have been identified in human tissues by mol...
journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1006/jmcc.1996.0184
更新日期：1996-09-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2019.09.006
更新日期：2019-11-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2004.05.013
更新日期：2004-08-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1006/jmcc.1996.0354
更新日期：1997-04-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2019.08.006
更新日期：2019-10-01 00:00:00
abstract：:Immediate post-receptor events following alpha-adrenoceptor stimulation in cardiac ventricular muscle are still largely unknown. Since membrane redox systems appear to be present in cell plasma membranes and may be involved in trans-sarcolemma electron efflux, the possibility that Ca2+ inflow was controlled by electro...
journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/s0022-2828(86)80462-x
更新日期：1986-11-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2007.12.008
更新日期：2008-03-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2004.06.014
更新日期：2004-09-01 00:00:00
abstract：:Catecholaminergic polymorphic ventricular tachycardia (CPVT) is linked to mutations in the cardiac ryanodine receptor (RyR2) or calsequestrin. We recently found that the drug flecainide inhibits RyR2 channels and prevents CPVT in mice and humans. Here we compared the effects of flecainide and tetracaine, a known RyR2 ...
journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2009.10.005
更新日期：2010-02-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2013.07.005
更新日期：2013-10-01 00:00:00
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journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/s0022-2828(08)80025-9
更新日期：1995-01-01 00:00:00
abstract：:Attenuation of excessive rates of myocardial glycolysis limits proton production and Ca(2+) overload during reperfusion and improves recovery of post-ischemic left ventricular (LV) function. In order to elucidate mechanisms underlying glycolytic inhibition by adenosine (ADO), this study tested the hypothesis that the ...
journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/j.yjmcc.2012.03.014
更新日期：2012-06-01 00:00:00
abstract：:Satellite cells from adult mouse tongue, diaphragm, vastus lateralis, rectus femoris, tibialis anterior, soleus, and extensor digitorum longus muscles were isolated, expanded, and differentiated under identical culture conditions. Proliferating myoblasts and differentiated myofiber cultures were analyzed via SDS-PAGE,...
journal_title：Journal of molecular and cellular cardiology
pub_type： 杂志文章
doi：10.1016/s0022-2828(03)00245-1
更新日期：2003-10-01 00:00:00
