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23 results on '"Bilio Marchesa"'

1. miRNeye: a microRNA expression atlas of the mouse eye

Author

Verde Roberta, Bilio Marchesa, Gennarino Vincenzo A, Peluso Ivana, Karali Marianthi, Lago Giampiero, Dollé Pascal, and Banfi Sandro

Subjects
Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background MicroRNAs (miRNAs) are key regulators of biological processes. To define miRNA function in the eye, it is essential to determine a high-resolution profile of their spatial and temporal distribution. Results In this report, we present the first comprehensive survey of miRNA expression in ocular tissues, using both microarray and RNA in situ hybridization (ISH) procedures. We initially determined the expression profiles of miRNAs in the retina, lens, cornea and retinal pigment epithelium of the adult mouse eye by microarray. Each tissue exhibited notably distinct miRNA enrichment patterns and cluster analysis identified groups of miRNAs that showed predominant expression in specific ocular tissues or combinations of them. Next, we performed RNA ISH for over 220 miRNAs, including those showing the highest expression levels by microarray, and generated a high-resolution expression atlas of miRNAs in the developing and adult wild-type mouse eye, which is accessible in the form of a publicly available web database. We found that 122 miRNAs displayed restricted expression domains in the eye at different developmental stages, with the majority of them expressed in one or more cell layers of the neural retina. Conclusions This analysis revealed miRNAs with differential expression in ocular tissues and provided a detailed atlas of their tissue-specific distribution during development of the murine eye. The combination of the two approaches offers a valuable resource to decipher the contributions of specific miRNAs and miRNA clusters to the development of distinct ocular structures.

Published
2010
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13. Left pulmonary artery in 22q11.2 deletion syndrome. Echocardiographic evaluation in patients without cardiac defects and role of Tbx1 in mice

Author

Mastromoro, Gioia, primary, Calcagni, Giulio, additional, Versacci, Paolo, additional, Putotto, Carolina, additional, Chinali, Marcello, additional, Lambiase, Caterina, additional, Unolt, Marta, additional, Pelliccione, Elena, additional, Anaclerio, Silvia, additional, Caprio, Cinzia, additional, Cioffi, Sara, additional, Bilio, Marchesa, additional, Baban, Anwar, additional, Drago, Fabrizio, additional, Digilio, Maria Cristina, additional, Marino, Bruno, additional, and Baldini, Antonio, additional

Published
2019
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18. Tbx1 regulates brain vascularization

Author

Cioffi, Sara, primary, Martucciello, Stefania, additional, Fulcoli, Filomena Gabriella, additional, Bilio, Marchesa, additional, Ferrentino, Rosa, additional, Nusco, Edoardo, additional, and Illingworth, Elizabeth, additional

Published
2013
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19. A High-Resolution Anatomical Atlas of the Transcriptome in the Mouse Embryo

Author

Diez-Roux, Graciana, primary, Banfi, Sandro, additional, Sultan, Marc, additional, Geffers, Lars, additional, Anand, Santosh, additional, Rozado, David, additional, Magen, Alon, additional, Canidio, Elena, additional, Pagani, Massimiliano, additional, Peluso, Ivana, additional, Lin-Marq, Nathalie, additional, Koch, Muriel, additional, Bilio, Marchesa, additional, Cantiello, Immacolata, additional, Verde, Roberta, additional, De Masi, Cristian, additional, Bianchi, Salvatore A., additional, Cicchini, Juliette, additional, Perroud, Elodie, additional, Mehmeti, Shprese, additional, Dagand, Emilie, additional, Schrinner, Sabine, additional, Nürnberger, Asja, additional, Schmidt, Katja, additional, Metz, Katja, additional, Zwingmann, Christina, additional, Brieske, Norbert, additional, Springer, Cindy, additional, Hernandez, Ana Martinez, additional, Herzog, Sarah, additional, Grabbe, Frauke, additional, Sieverding, Cornelia, additional, Fischer, Barbara, additional, Schrader, Kathrin, additional, Brockmeyer, Maren, additional, Dettmer, Sarah, additional, Helbig, Christin, additional, Alunni, Violaine, additional, Battaini, Marie-Annick, additional, Mura, Carole, additional, Henrichsen, Charlotte N., additional, Garcia-Lopez, Raquel, additional, Echevarria, Diego, additional, Puelles, Eduardo, additional, Garcia-Calero, Elena, additional, Kruse, Stefan, additional, Uhr, Markus, additional, Kauck, Christine, additional, Feng, Guangjie, additional, Milyaev, Nestor, additional, Ong, Chuang Kee, additional, Kumar, Lalit, additional, Lam, MeiSze, additional, Semple, Colin A., additional, Gyenesei, Attila, additional, Mundlos, Stefan, additional, Radelof, Uwe, additional, Lehrach, Hans, additional, Sarmientos, Paolo, additional, Reymond, Alexandre, additional, Davidson, Duncan R., additional, Dollé, Pascal, additional, Antonarakis, Stylianos E., additional, Yaspo, Marie-Laure, additional, Martinez, Salvador, additional, Baldock, Richard A., additional, Eichele, Gregor, additional, and Ballabio, Andrea, additional

Published
2011
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20. miRNeye: a microRNA expression atlas of themouse eye.

Author

Karali, Marianthi, Peluso, Ivana, Gennarino, Vincenzo A., Bilio, Marchesa, Verde, Roberta, Lago, Giampiero, Dollé, Pascal, and Banfi, Sandro

Subjects
CRYOBIOLOGY, VITAMIN A, RETINAL (Visual pigment), POSTERIOR segment (Eye), WEB databases
Abstract

Background: MicroRNAs (miRNAs) are key regulators of biological processes. To define miRNA function in the eye, it is essential to determine a high-resolution profile of their spatial and temporal distribution. Results: In this report, we present the first comprehensive survey of miRNA expression in ocular tissues, using both microarray and RNA in situ hybridization (ISH) procedures. We initially determined the expression profiles of miRNAs in the retina, lens, cornea and retinal pigment epithelium of the adult mouse eye by microarray. Each tissue exhibited notably distinct miRNA enrichment patterns and cluster analysis identified groups of miRNAs that showed predominant expression in specific ocular tissues or combinations of them. Next, we performed RNA ISH for over 220 miRNAs, including those showing the highest expression levels by microarray, and generated a highresolution expression atlas of miRNAs in the developing and adult wild-type mouse eye, which is accessible in the form of a publicly available web database. We found that 122 miRNAs displayed restricted expression domains in the eye at different developmental stages, with the majority of them expressed in one or more cell layers of the neural retina. Conclusions: This analysis revealed miRNAs with differential expression in ocular tissues and provided a detailed atlas of their tissue-specific distribution during development of the murine eye. The combination of the two approaches offers a valuable resource to decipher the contributions of specific miRNAs and miRNA clusters to the development of distinct ocular structures. [ABSTRACT FROM AUTHOR]

Published
2010
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21. EZH2 is required for parathyroid and thymic development through differentiation of the third pharyngeal pouch endoderm

Author

Cinzia Caprio, Gabriella Lania, Li Chen, Rosa Ferrentino, Marchesa Bilio, Antonio Baldini, Caprio, Cinzia, Lania, Gabriella, Bilio, Marchesa, Ferrentino, Rosa, Chen, Li, and Baldini, Antonio

Subjects
TBX1, Parathyroid, Pharyngeal pouch, Organogenesis, parathyroids, Neuroscience (miscellaneous), Medicine (miscellaneous), ezh2, macromolecular substances, Biology, General Biochemistry, Genetics and Molecular Biology, Histone H3, Mice, Immunology and Microbiology (miscellaneous), stomatognathic system, Pharyngeal apparatus, medicine, Morphogenesis, Pathology, Animals, RB1-214, EZH2, Endoderm, FOXN1, Gene Expression Regulation, Developmental, Cell Differentiation, Cell biology, medicine.anatomical_structure, Histone methyltransferase, pharyngeal endoderm, embryonic structures, tbx1, Medicine, T-Box Domain Proteins, Research Article
Abstract

The Ezh2 gene encodes a histone methyltransferase of the polycomb repressive complex 2 that methylates histone H3 lysine 27. In this study, we investigated whether EZH2 has a role in the development of the pharyngeal apparatus and whether it regulates the expression of the Tbx1 gene, which encodes a key transcription factor required in pharyngeal development. To these ends, we performed genetic in vivo experiments with mouse embryos and used mouse embryonic stem cell (ESC)-based protocols to probe endoderm and cardiogenic mesoderm differentiation. Results showed that EZH2 occupies the Tbx1 gene locus in mouse embryos, and that suppression of EZH2 was associated with reduced expression of Tbx1 in differentiated mouse ESCs. Conditional deletion of Ezh2 in the Tbx1 expression domain, which includes the pharyngeal endoderm, did not cause cardiac defects but revealed that the gene has an important role in the morphogenesis of the third pharyngeal pouch (PP). We found that in conditionally deleted embryos the third PP was hypoplastic, had reduced expression of Tbx1, lacked the expression of Gcm2, a gene that marks the parathyroid domain, but expressed FoxN1, a gene marking the thymic domain. Consistently, the parathyroids did not develop, and the thymus was hypoplastic. Thus, Ezh2 is required for parathyroid and thymic development, probably through a function in the pouch endoderm. This discovery also provides a novel interpretational key for the finding of Ezh2 activating mutations in hyperparathyroidism and parathyroid cancer., Summary: EZH2 in the pharyngeal apparatus is required in the endoderm for the development of the parathyroids and thymus, and positively regulates the expression of the Tbx1 gene.

Published
2021

22. TBX1 and Basal Cell Carcinoma: Expression and Interactions with Gli2 and Dvl2 Signaling

Author

Marchesa Bilio, Cinzia Caprio, Gennaro Ilardi, Daniela Alfano, Stefania Staibano, Antonio Baldini, Federica Feo, Rosa Ferrentino, Daniela Russo, Silvia Varricchio, Caterina Missero, Caprio, Cinzia, Varricchio, Silvia, Bilio, Marchesa, Feo, Federica, Ferrentino, Rosa, Russo, Daniela, Staibano, Stefania, Alfano, Daniela, Missero, Caterina, Ilardi, Gennaro, and Baldini, Antonio

Subjects
animal structures, T-box transcription factor TBX1, basal cell carcinoma, genetic marker, Biology, Fibroblast growth factor, Catalysis, Inorganic Chemistry, lcsh:Chemistry, 03 medical and health sciences, 0302 clinical medicine, stomatognathic system, GLI2, Physical and Theoretical Chemistry, Progenitor cell, Molecular Biology, Transcription factor, lcsh:QH301-705.5, Spectroscopy, 030304 developmental biology, 0303 health sciences, integumentary system, Cell growth, Organic Chemistry, Wnt signaling pathway, Signal transducing adaptor protein, t-box transcription factor tbx1, General Medicine, Computer Science Applications, Cell biology, lcsh:Biology (General), lcsh:QD1-999, 030220 oncology & carcinogenesis, embryonic structures, Smoothened
Abstract

Early events of basal cell carcinoma (BCC) tumorigenesis are triggered by inappropriate activation of SHH signaling, via the loss of Patched1 (Ptch1) or by activating mutations of Smoothened (Smo). TBX1 is a key regulator of pharyngeal development, mainly through expression in multipotent progenitor cells of the cardiopharyngeal lineage. This transcription factor is connected to several major signaling systems, such as FGF, WNT, and SHH, and it has been linked to cell proliferation and to the regulation of cell shape and cell dynamics. Here, we show that TBX1 was expressed in all of the 51 BCC samples that we have tested, while in healthy human skin it was only expressed in the hair follicle. Signal intensity and distribution was heterogeneous among tumor samples. Experiments performed on a cellular model of mouse BCC showed that Tbx1 is downstream to GLI2, a factor in the SHH signaling, and that, in turn, it regulates the expression of Dvl2, which encodes an adaptor protein that is necessary for the transduction of WNT signaling. Consistently, Tbx1 depletion in the cellular model significantly reduced cell migration. These results suggest that TBX1 is part of a core transcription network that promotes BCC tumorigenesis.

Published
2020

23. Tbx1 represses Mef2c gene expression and is correlated with histone 3 deacetylation of the anterior heart field enhancer

Author

Alessandra Altomonte, Luna Simona Pane, Andrea Cirino, Rosa Ferrentino, Filomena Gabriella Fulcoli, Marchesa Bilio, Antonio Baldini, Pane, Luna Simona, Fulcoli, Filomena Gabriella, Cirino, Andrea, Altomonte, Alessandra, Ferrentino, Rosa, Bilio, Marchesa, and Baldini, Antonio

Subjects
0301 basic medicine, Medicine (miscellaneous), lcsh:Medicine, Histones, 0302 clinical medicine, Immunology and Microbiology (miscellaneous), MEF2C Gene, MEF2C, MEF2 Transcription Factors, Gene Expression Regulation, Developmental, Acetylation, Cell Differentiation, Heart, Tbx1, Cell biology, Anterior heart field enhancer, Mef2c, Histone, Enhancer Elements, Genetic, embryonic structures, Female, Research Article, lcsh:RB1-214, TBX1, Transgene, Induced Pluripotent Stem Cells, Neuroscience (miscellaneous), Mice, Transgenic, Biology, General Biochemistry, Genetics and Molecular Biology, Cell Line, 03 medical and health sciences, stomatognathic system, DiGeorge Syndrome, lcsh:Pathology, Animals, Humans, Enhancer, Transcription factor, Biochemistry, Genetics and Molecular Biology (all), Base Sequence, Myocardium, lcsh:R, Embryo, Mammalian, GATA4 Transcription Factor, 030104 developmental biology, biology.protein, T-Box Domain Proteins, 030217 neurology & neurosurgery
Abstract

The TBX1 gene is haploinsufficient in 22q11.2 deletion syndrome (22q11.2DS), and genetic evidence from human patients and mouse models points to a major role of this gene in the pathogenesis of this syndrome. Tbx1 can activate and repress transcription, and previous work has shown that one of its functions is to negatively modulate cardiomyocyte differentiation. Tbx1 occupies the anterior heart field (AHF) enhancer of the Mef2c gene, which encodes a key cardiac differentiation transcription factor. Here, we show that increased dosage of Tbx1 correlates with downregulation of Mef2c expression and reduced acetylation of its AHF enhancer in cultured mouse myoblasts. Consistently, 22q11.2DS-derived and in vitro-differentiated human induced pluripotent stem cells (hiPSCs) expressed higher levels of MEF2C and showed increased AHF acetylation, compared with hiPSCs from a healthy donor. Most importantly, we show that in mouse embryos, loss of Tbx1 enhances the expression of the Mef2c-AHF-Cre transgene in a specific region of the splanchnic mesoderm, and in a dosage-dependent manner, providing an in vivo correlate of our cell culture data. These results indicate that Tbx1 regulates the Mef2c AHF enhancer by inducing histone deacetylation., Summary: Using three experimental models, we demonstrate that Tbx1 suppresses Mef2c gene expression, and show that histone 3 acetylation of the anterior heart field enhancer of the Mef2c gene responds negatively to Tbx1 dosage.

Published
2018

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