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Limana F.,Centro Cardiologico Monzino | Capogrossi M.C.,Laboratorio Of Patologia Vascolare | Germani A.,Fondazione Livio Patrizi
Pharmacology and Therapeutics | Year: 2011

During heart development, the epicardium provides cardiogenic progenitor cells and, together with the myocardium, directs lineage specification and coordinates both myocardial growth and coronary vasculature formation. In the adult heart, the established function of the epicardium is to provide a smooth surface that, together with the pericardium, favors heart movement during contraction and relaxation. Recently, epicardial precursor cells with the ability to differentiate into cardiomyocytes and vascular cells have been identified and the quiescent nature of the adult epicardium has been questioned. Interestingly, the signaling pathways involved in this process appear to be regulated, in the adult heart, by mechanisms similar to those in the embryonic heart. This review will summarize the properties of the embryonic epicardium and will focus on recent advances on the role of the adult epicardium in cardiac regeneration. Specifically, we will present aspects of epicardial cell biology that may be relevant to the development of new therapeutic approaches aimed at inducing heart repair following injury. © 2010 Elsevier Inc. All rights reserved. Source

Giardina E.,University of Rome Tor Vergata | Stocchi L.,University of Rome Tor Vergata | Cuzzola V.F.,IRCCS Centro Neurolesi Bonino Pulejo | Zampatti S.,University of Rome Tor Vergata | And 6 more authors.
Electrophoresis | Year: 2010

Abacavir (ABC) is an antiretroviral drug highly effective in the treatment of HIV, but its intake can cause severe hypersensitivity reaction (HSR). A strong association between HLA-B*57:01 and ABC HSRs was reported by several studies, which demonstrated that HLA-B*57:01 screening had a 100% negative predictive value and that it could accurately identify patients at high risk of ABC HSRs. We propose a new sequence-specific primer PCR assay based on fluorescence detection through CE which is highly sensitive, allowing the use of non-infective sources of DNA such as saliva and buccal swabs, in addition to blood and reproducible, allowing automation of the analytical process. The results of our study were first compared with a standard sequence-specific primer PCR technique and reported a concordance of 100%, and then a blind external validation further confirmed the accuracy of our method. © 2010 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. Source

Limana F.,Centro Cardiologico Monzino | Bertolami C.,Laboratorio Of Patologia Vascolare | Mangoni A.,Laboratorio Of Patologia Vascolare | Di Carlo A.,Laboratorio Of Patologia Vascolare | And 8 more authors.
Journal of Molecular and Cellular Cardiology | Year: 2010

Stem cells expressing c-kit have been identified in the adult epicardium. In mice, after myocardial infarction, these cells proliferate, migrate to the injury site and differentiate toward myocardial and vascular phenotype. We hypothesized that, acutely after myocardial infarction, pericardial sac integrity and pericardial fluid (PF) may play a role on epicardial cell gene expression, proliferation and differentiation. Microarray analysis indicated that, in the presence of an intact pericardial sac, myocardial infarction modulated 246 genes in epicardial cells most of which were related to cell proliferation, cytoskeletal organization, wound repair and signal transduction. Interestingly, WT1, Tbx18 and RALDH2, notably involved in epicardial embryonic development, were markedly up-regulated. Importantly, coexpression of stem cell antigen c-kit and WT1 and/or Tbx18 was detected by immunohistochemistry in the mouse epicardium during embryogenesis as well as in adult mouse infarcted heart. Injection of human pericardial fluid from patients with acute myocardial ischemia (PFMI) in the pericardial cavity of non-infarcted mouse hearts, enhanced, epicardial cell proliferation and WT1 expression. Further, PFMI supplementation to hypoxic cultured human epicardial c-kit+ cells increased WT1 and Tbx18 mRNA expression. Finally, insulin-like growth factor 1, hepatocyte growth factor and high mobility group box 1 protein, previously involved in cardiac c-kit+ cell proliferation and differentiation, were increased in PFMI compared to the pericardial fluid of non ischemic patients. In conclusion, myocardial infarction reactivates an embryonic program in epicardial c-kit+ cells; soluble factors released in the pericardial fluids following myocardial necrosis may play a role in this process. © 2009 Elsevier Ltd. All rights reserved. Source

Rossini A.,Centro Cardiologico Monzino | Rossini A.,University of Milan | Frati C.,University of Parma | Lagrasta C.,University of Parma | And 18 more authors.
Cardiovascular Research | Year: 2011

AimsBone marrow mesenchymal stromal cell (BMStC) transplantation into the infarcted heart improves left ventricular function and cardiac remodelling. However, it has been suggested that tissue-specific cells may be better for cardiac repair than cells from other sources. The objective of the present work has been the comparison of in vitro and in vivo properties of adult human cardiac stromal cells (CStC) to those of syngeneic BMStC.Methods and resultsAlthough CStC and BMStC exhibited a similar immunophenotype, their gene, microRNA, and protein expression profiles were remarkably different. Biologically, CStC, compared with BMStC, were less competent in acquiring the adipogenic and osteogenic phenotype but more efficiently expressed cardiovascular markers. When injected into the heart, in rat a model of chronic myocardial infarction, CStC persisted longer within the tissue, migrated into the scar, and differentiated into adult cardiomyocytes better than BMStC.ConclusionOur findings demonstrate that although CStC and BMStC share a common stromal phenotype, CStC present cardiovascular-associated features and may represent an important cell source for more efficient cardiac repair. © 2010 The Author. Source

Conte C.,University of Rome Tor Vergata | D'Apice M.R.,University of Rome Tor Vergata | Rinaldi F.,University of Rome Tor Vergata | Gambardella S.,Fondazione Livio Patrizi | And 2 more authors.
BMC Medical Genetics | Year: 2011

Background: Treacher Collins syndrome (TCS) is one of the most severe autosomal dominant congenital disorders of craniofacial development and shows variable phenotypic expression. TCS is extremely rare, occurring with an incidence of 1 in 50.000 live births. The TCS distinguishing characteristics are represented by down slanting palpebral fissures, coloboma of the eyelid, micrognathia, microtia and other deformity of the ears, hypoplastic zygomatic arches, and macrostomia. Conductive hearing loss and cleft palate are often present. TCS results from mutations in the TCOF1 gene located on chromosome 5, which encodes a serine/alanine-rich nucleolar phospho-protein called Treacle. However, alterations in the TCOF1 gene have been implicated in only 81-93% of TCS cases.Methods: In this study, the entire coding regions of the TCOF1 gene, including newly described exons 6A and 16A, were sequenced in 46 unrelated subjects suspected of TCS clinical indication.Results: Fifteen mutations were reported, including twelve novel and three already described in 14 sporadic patients and in 3 familial cases. Moreover, seven novel polymorphisms were also described. Most of the mutations characterised were microdeletions spanning one or more nucleotides, in addition to an insertion of one nucleotide in exon 18 and a stop mutation. The deletions and the insertion described cause a premature termination of translation, resulting in a truncated protein.Conclusion: This study confirms that almost all the TCOF1 pathogenic mutations fall in the coding region and lead to an aberrant protein. © 2011 Conte et al; licensee BioMed Central Ltd. Source

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