Publications
370 results found
Temmerman L, Slonimsky E, Rosenthal N, 2010, Class 2 IGF-1 isoforms are dispensable for viability, growth and maintenance of IGF-1 serum levels, GROWTH HORMONE & IGF RESEARCH, Vol: 20, Pages: 255-263, ISSN: 1096-6374
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- Citations: 26
Zouberakis M, Chandras C, Swertz M, et al., 2010, Mouse resource browser-a database of mouse databases, Database: the journal of biological databases and curation, Vol: 2010, Pages: 1-7, ISSN: 1758-0463
The laboratory mouse has become the organism of choice for discovering gene function and unravelling pathogenetic mechanisms of human diseases through the application of various functional genomic approaches. The resulting deluge of data has led to the deployment of numerous online resources and the concomitant need for formalized experimental descriptions, data standardization, database interoperability and integration, a need that has yet to be met. We present here the Mouse Resource Browser (MRB), a database of mouse databases that indexes 217 publicly available mouse resources under 22 categories and uses a standardised database description framework (the CASIMIR DDF) to provide information on their controlled vocabularies (ontologies and minimum information standards), and technical information on programmatic access and data availability. Focusing on interoperability and integration, MRB offers automatic generation of downloadable and re-distributable SOAP application-programming interfaces for resources that provide direct database access. MRB aims to provide useful information to both bench scientists, who can easily navigate and find all mouse related resources in one place, and bioinformaticians, who will be provided with interoperable resources containing data which can be mined and integrated.
Bilbao D, Semenova E, Rosenthal N, 2010, Overexpression of mIGF-1 in keratinocytes protects hair follicles from alopecia in mice, Annual Meeting of the British-Society-for-Investigative-Dermatology, Publisher: WILEY-BLACKWELL PUBLISHING, INC, Pages: 930-931, ISSN: 0007-0963
Vinciguerra M, Fulco M, Ladurner A, et al., 2010, SirT1 in muscle physiology and disease: lessons from mouse models, DISEASE MODELS & MECHANISMS, Vol: 3, Pages: 298-303, ISSN: 1754-8403
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- Citations: 47
Shavlakadze T, Chai J, Maley K, et al., 2010, A growth stimulus is needed for IGF-1 to induce skeletal muscle hypertrophy in vivo, JOURNAL OF CELL SCIENCE, Vol: 123, Pages: 960-971, ISSN: 0021-9533
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- Citations: 71
Kratsios P, Catela C, Salimova E, et al., 2010, Distinct Roles for Cell-Autonomous Notch Signaling in Cardiomyocytes of the Embryonic and Adult Heart, CIRCULATION RESEARCH, Vol: 106, Pages: 559-572, ISSN: 0009-7330
Rationale: The Notch signaling pathway is important for cell-cell communication that controls tissue formation and homeostasis during embryonic and adult life, but the precise cell targets of Notch signaling in the mammalian heart remain poorly defined.Objective: To investigate the functional role of Notch signaling in the cardiomyocyte compartment of the embryonic and adult heart.Methods and Results: Here, we report that either conditional overexpression of Notch1 intracellular domain (NICD1) or selective silencing of Notch signaling in the embryonic cardiomyocyte compartment results in developmental defects and perinatal lethality. In contrast, augmentation of endogenous Notch reactivation after myocardial infarction in the adult, either by inducing cardiomyocyte-specific Notch1 transgene expression or by intramyocardial delivery of a Notch1 pseudoligand, increases survival rate, improves cardiac functional performance, and minimizes fibrosis, promoting antiapoptotic and angiogenic mechanisms.Conclusions: These results reveal a strict requirement for cell-autonomous modulation of Notch signaling during heart morphogenesis, and illustrate how the same signaling pathway that promotes congenital heart defects when perturbed in the embryo can be therapeutically redeployed for the treatment of adult myocardial damage. (Circ Res. 2010;106:559-572.)
Castillo HA, Cravo RM, Azambuja AP, et al., 2010, Insights into the organization of dorsal spinal cord pathways from an evolutionarily conserved <i>raldh2</i> intronic enhancer, DEVELOPMENT, Vol: 137, Pages: 507-518, ISSN: 0950-1991
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- Citations: 21
Mandillo M, Tucci V, Hoelter SM, et al., 2010, Reliability, robustness, and reproducibility in mouse behavioral phenotyping: a cross-laboratory study. (vol 34, pg 243, 2008), PHYSIOLOGICAL GENOMICS, Vol: 40, Pages: 217-217, ISSN: 1094-8341
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- Citations: 1
Kratsios P, Huth M, Temmerman L, et al., 2010, Antioxidant Amelioration of Dilated Cardiomyopathy Caused by Conditional Deletion of NEMO/IKKγ in Cardiomyocytes, CIRCULATION RESEARCH, Vol: 106, Pages: 133-144, ISSN: 0009-7330
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- Citations: 49
Lara-Pezzi E, Rosenthal N, 2010, Genetic Enhancement of Cardiac Regeneration, Heart Development and Regeneration: Volume I, Pages: 981-997, ISBN: 9780123813329
This chapter describes emerging genetic strategies for enhancing self-renewal in cardiac pathologies. Although effective cell-based repair of the mammalian heart is now a feasible goal of regenerative medicine, further investigation is necessary to improve the very poor graft survival and rate of proliferation of cells after injection, and to exploit their capacities to transdifferentiate, integrate, or protect the remaining myocardium. Stimulation of proliferation using cell-cycle components or growth factors has been successfully applied to regeneration of damaged mammalian tissues in animal models. Manipulation of extracellular matrix composition may also provide a better regenerative environment in the damaged heart. Enhancement of the heart's inherent, although limited, capacity to regenerate by manipulating gene expression is a necessary prerequisite for translation into a viable therapy. However, many of the approaches that have succeeded in enhancing cardiac regeneration have used transgenic mice as research models. Clinical application of these genetic strategies faces the same hurdles as any gene therapeutic protocol. Whether the regenerative agent is a gene or a recombinant protein, the choice of its delivery route to the damaged myocardium is determined by the safety of the treatment and its efficacy. The most recent advances that may exploit combinations of cell and genetic therapies are also reviewed in this chapter.
Morgan H, Beck T, Blake A, et al., 2010, EuroPhenome: a repository for high-throughput mouse phenotyping data, Nucleic Acids Research, Vol: 38, Pages: D577-D585, ISSN: 0305-1048
The broad aim of biomedical science in the postgenomic era is to link genomic and phenotype information to allow deeper understanding of the processes leading from genomic changes to altered phenotype and disease. The EuroPhenome project (http://www.EuroPhenome.org) is a comprehensive resource for raw and annotated high-throughput phenotyping data arising from projects such as EUMODIC. EUMODIC is gathering data from the EMPReSSslim pipeline (http://www.empress.har.mrc.ac.uk/) which is performed on inbred mouse strains and knock-out lines arising from the EUCOMM project. The EuroPhenome interface allows the user to access the data via the phenotype or genotype. It also allows the user to access the data in a variety of ways, including graphical display, statistical analysis and access to the raw data via web services. The raw phenotyping data captured in EuroPhenome is annotated by an annotation pipeline which automatically identifies statistically different mutants from the appropriate baseline and assigns ontology terms for that specific test. Mutant phenotypes can be quickly identified using two EuroPhenome tools: PhenoMap, a graphical representation of statistically relevant phenotypes, and mining for a mutant using ontology terms. To assist with data definition and cross-database comparisons, phenotype data is annotated using combinations of terms from biological ontologies.
Vinciguerra M, Santini MP, Claycomb WC, et al., 2010, Local IGF-1 isoform protects cardiomyocytes from hypertrophic and oxidative stresses via SirT1 activity, AGING-US, Vol: 2, Pages: 43-62, ISSN: 1945-4589
Oxidative and hypertrophic stresses contribute to the pathogenesis of heart failure. Insulin-like growth factor-1 (IGF-1) is a peptide hormone with a complex post-transcriptional regulation, generating distinct isoforms. Locally acting IGF-1 isoform (mIGF-1) helps the heart to recover from toxic injury and from infarct. In the murine heart, moderate overexpression of the NAD+-dependent deacetylase SirT1 was reported to mitigate oxidative stress. SirT1 is known to promote lifespan extension and to protect from metabolic challenges. Circulating IGF-1 and SirT1 play antagonizing biological roles and share molecular targets in the heart, in turn affecting cardiomyocyte physiology. However, how different IGF-1 isoforms may impact SirT1 and affect cardiomyocyte function is unknown. Here we show that locally acting mIGF-1 increases SirT1 expression/activity, whereas circulating IGF-1 isoform does not affect it, in cultured HL-1 and neonatal cardiomyocytes. mIGF-1-induced SirT1 activity exerts protection against angiotensin II (Ang II)-triggered hypertrophy and against paraquat (PQ) and Ang II-induced oxidative stress. Conversely, circulating IGF-1 triggered itself oxidative stress and cardiomyocyte hypertrophy. Interestingly, potent cardio-protective genes (adiponectin, UCP-1 and MT-2) were increased specifically in mIGF-1-overexpressing cardiomyocytes, in a SirT1-dependent fashion. Thus, mIGF-1 protects cardiomyocytes from oxidative and hypertrophic stresses via SirT1 activity, and may represent a promising cardiac therapeutic.
Rosenthal N, Harvey RP, 2010, Heart Development and Regeneration, ISBN: 9780123813329
The development of the cardiovascular system is a rapidly advancing area in biomedical research, now coupled with the burgeoning field of cardiac regenerative medicine. A lucid understanding of these fields is paramount to reducing human cardiovascular diseases of both fetal and adult origin. Significant progress can now be made through a comprehensive investigation of embryonic development and its genetic control circuitry. Heart Development and Regeneration, written by experts in the field, provides essential information on topics ranging from the evolution and lineage origins of the developing cardiovascular system to cardiac regenerative medicine. A reference for clinicians, medical researchers, students, and teachers, this publication offers broad coverage of the most recent advances. Volume One discusses heart evolution, contributing cell lineages; model systems; cardiac growth; morphology and asymmetry; heart patterning; epicardial, vascular, and lymphatic development; and congenital heart diseases. Volume Two includes chapters on transcription factors and transcriptional control circuits in cardiac development and disease; epigenetic modifiers including microRNAs, genome-wide mutagenesis, imaging, and proteomics approaches; and the theory and practice of stem cells and cardiac regeneration.
Rosenthal N, Costa MA, 2010, Unravelling the endovascular microenvironment by optical coherence tomography, EUROPEAN HEART JOURNAL, Vol: 31, Pages: 139-142, ISSN: 0195-668X
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- Citations: 5
Vinciguerra M, Musaro A, Rosenthal N, 2010, Regulation of Muscle Atrophy in Aging and Disease, PROTEIN METABOLISM AND HOMEOSTASIS IN AGING, Editors: Tavernarakis, Publisher: SPRINGER-VERLAG BERLIN, Pages: 211-233, ISBN: 978-1-4419-7001-5
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- Citations: 112
Brand NJ, Lara-Pezzi E, Rosenthal N, et al., 2010, Analysis of Cardiac Myocyte Biology in Transgenic Mice: A Protocol for Preparation of Neonatal Mouse Cardiac Myocyte Cultures, MOUSE CELL CULTURE: METHODS AND PROTOCOLS, Vol: 633, Pages: 113-124, ISSN: 1064-3745
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- Citations: 16
Chandras C, Weaver T, Zouberakis M, et al., 2009, Models for financial sustainability of biological databases and resources, Database: the journal of biological databases and curation, Vol: 2009, Pages: 1-9, ISSN: 1758-0463
Following the technological advances that have enabled genome-wide analysis in most model organisms over the last decade, there has been unprecedented growth in genomic and post-genomic science with concomitant generation of an exponentially increasing volume of data and material resources. As a result, numerous repositories have been created to store and archive data, organisms and material, which are of substantial value to the whole community. Sustained access, facilitating re-use of these resources, is essential, not only for validation, but for re-analysis, testing of new hypotheses and developing new technologies/platforms. A common challenge for most data resources and biological repositories today is finding financial support for maintenance and development to best serve the scientific community. In this study we examine the problems that currently confront the data and resource infrastructure underlying the biomedical sciences. We discuss the financial sustainability issues and potential business models that could be adopted by biological resources and consider long term preservation issues within the context of mouse functional genomics efforts in Europe.
Ruffell D, Mourkioti F, Gambardella A, et al., 2009, A CREB-C/EBPβ cascade induces M2 macrophage-specific gene expression and promotes muscle injury repair, PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, Vol: 106, Pages: 17475-17480, ISSN: 0027-8424
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- Citations: 451
Schofield PN, Bubela T, Weaver T, et al., 2009, Post-publication sharing of data and tools, NATURE, Vol: 461, Pages: 171-173, ISSN: 0028-0836
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- Citations: 103
Rosenthal N, Yacoub M, 2009, Taking translational research to heart: an interview with Sir Magdi Yacoub, DISEASE MODELS & MECHANISMS, Vol: 2, Pages: 433-435, ISSN: 1754-8403
Catela C, Bilbao-Cortes D, Slonimsky E, et al., 2009, A role for fibroblast growth factor receptor - like 1 in Wolf-Hirschhorn syndrome, 16th Annual Conference of the International-Society-of-Development-Biologists, Publisher: ELSEVIER SCIENCE BV, Pages: S133-S134, ISSN: 0925-4773
Rosenthal N, 2009, Enhancing mammalian regeneration, 16th Annual Conference of the International-Society-of-Development-Biologists, Publisher: ELSEVIER SCIENCE BV, Pages: S2-S2, ISSN: 0925-4773
Catela C, Bilbao-Cortes D, Slonimsky E, et al., 2009, Multiple congenital malformations of Wolf-Hirschhorn syndrome are recapitulated in <i>Fgfrl1</i> null mice, DISEASE MODELS & MECHANISMS, Vol: 2, Pages: 283-294, ISSN: 1754-8403
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- Citations: 71
Dobrowolny G, Aucello M, Rizzuto E, et al., 2009, Skeletal Muscle Is a Primary Target of SOD1<sup>G93A</sup>-Mediated Toxicity (DOI:10.1016/j.cmet.2008.09.002), Cell Metabolism, Vol: 9, ISSN: 1550-4131
Santini MP, Poudel B, Rosenthal N, 2009, Stem Cells and the Regenerating Heart, ESSENTIALS OF STEM CELL BIOLOGY, 2ND EDITION, Editors: Lanza, Gearhart, Hogan, Melton, Pedersen, Thomas, Thomson, Wilmut, Publisher: ELSEVIER SCIENCE BV, Pages: 259-263
Rosenthal N, 2009, ENHANCING MAMMALIAN REGENERATION, Publisher: SPRINGER TOKYO, Pages: 12-12, ISSN: 1880-6546
Dobrowolny G, Aucello M, Rizzuto E, et al., 2008, Skeletal Muscle Is a Primary Target of SOD1<SUP>G93A</SUP>-Mediated Toxicity, CELL METABOLISM, Vol: 8, Pages: 425-436, ISSN: 1550-4131
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- Citations: 380
Lara-Pezzi E, Felkin LE, Birks EJ, et al., 2008, Expression of Follistatin-Related Genes Is Altered in Heart Failure, ENDOCRINOLOGY, Vol: 149, Pages: 5822-5827, ISSN: 0013-7227
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- Citations: 66
Semenova E, Koegel H, Hasse S, et al., 2008, Overexpression of mIGF-1 in Keratinocytes Improves Wound Healing and Accelerates Hair Follicle Formation and Cycling in Mice, AMERICAN JOURNAL OF PATHOLOGY, Vol: 173, Pages: 1295-1310, ISSN: 0002-9440
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- Citations: 50
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