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Mouse Embryonic Development (mouse + embryonic_development)
Selected AbstractsSSAO/VAP-1 protein expression during mouse embryonic developmentDEVELOPMENTAL DYNAMICS, Issue 9 2008Tony Valente Abstract SSAO/VAP-1 is a multifunctional enzyme depending on in which tissue it is expressed. SSAO/VAP-1 is present in almost all adult mammalian tissues, especially in highly vascularised ones and in adipocytes. SSAO/VAP-1 is an amine oxidase able to metabolise various endogenous or exogenous primary amines. Its catalytic activity can lead to cellular oxidative stress, which has been implicated in several pathologies (atherosclerosis, diabetes, and Alzheimer's disease). The aim of this work is to achieve a study of SSAO/VAP-1 protein expression during mouse embryogenesis. Our results show that SSAO/VAP-1 appears early in the development of the vascular system, adipose tissue, and smooth muscle cells. Moreover, its expression is strong in several epithelia of the sensory organs, as well as in the development of cartilage sites. Altogether, this suggests that SSAO/VAP-1 enzyme could be involved in the differentiation processes that take place during embryonic development, concretely in tissue vascularisation. Developmental Dynamics 237:2585,2593, 2008. © 2008 Wiley-Liss, Inc. [source] Generation and analysis of a mouse line harboring GFP in the Eomes/Tbr2 locusGENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 11 2009Sebastian J. Arnold Abstract During mouse embryonic development, the T-box transcription factor Eomes/Tbr2 is expressed in highly dynamic patterns in various progenitor cell types. Those include the undifferentiated cells of the trophectoderm, ingressing nascent mesoderm at the primitive streak, and intermediate progenitor cells of the developing cerebral cortex. We generated an EomesGFP - targeted allele to follow the highly dynamic patterns of Eomes expression and to allow for the identification of novel expression domains. We show that our novel allele recapitulates endogenous gene expression at known sites of expression and confirm our results by anti-Eomes immunofluorescent staining. Using this novel allele we were able to identify previously undocumented domains of Eomes expression within the visceral endoderm and at various locations in the developing and adult mouse brain. genesis 47:775,781, 2009. © 2009 Wiley-Liss, Inc. [source] Foxf1 +/, mice exhibit defective stellate cell activation and abnormal liver regeneration following CCl4 injuryHEPATOLOGY, Issue 1 2003Vladimir V. Kalinichenko Previous studies have shown that haploinsufficiency of the splanchnic and septum transversum mesoderm Forkhead Box (Fox) f1 transcriptional factor caused defects in lung and gallbladder development and that Foxf1 heterozygous (+/,) mice exhibited defective lung repair in response to injury. In this study, we show that Foxf1 is expressed in hepatic stellate cells in developing and adult liver, suggesting that a subset of stellate cells originates from septum transversum mesenchyme during mouse embryonic development. Because liver regeneration requires a transient differentiation of stellate cells into myofibroblasts, which secrete type I collagen into the extracellular matrix, we examined Foxf1 +/, liver repair following carbon tetrachloride injury, a known model for stellate cell activation. We found that regenerating Foxf1 +/, liver exhibited defective stellate cell activation following CCl4 liver injury, which was associated with diminished induction of type I collagen, ,,smooth muscle actin, and Notch-2 protein and resulted in severe hepatic apoptosis despite normal cellular proliferation rates. Furthermore, regenerating Foxf1 +/, livers exhibited decreased levels of interferon-inducible protein 10 (IP-10), delayed induction of monocyte chemoattractant protein 1 (MCP-1) levels, and aberrantly elevated expression of transforming growth factor ,1. In conclusion, Foxf1 +/, mice exhibited abnormal liver repair, diminished activation of hepatic stellate cells, and increased pericentral hepatic apoptosis following CCl4 injury. [source] Barx1 and evolutionary changes in feedingJOURNAL OF ANATOMY, Issue 5 2005Isabelle Miletich Abstract During mouse embryonic development, the Barx1 homeobox gene is expressed in the mesenchymal cells of molar teeth and stomach. During early stages of molar development, Barx1 has an instructive role, directing the as yet undetermined ectomesenchymal cells in the proximal region of the jaws to follow a multicuspid tooth developmental pathway. We review here recent results showing an absence of stomach tissue in Barx1 mutant mice. The data strongly suggest that in the presumptive stomach mesenchyme Barx1 acts to attenuate Wnt signalling allowing digestive tract endoderm to differentiate into a highly specialized stomach epithelium. In the light of these new data, we discuss the possibility that evolutionary changes in the Barx1 gene could have simultaneously altered the dentition and the digestive system, therefore positioning Barx1 as a key gene in the evolution of mammals. [source] Mice deficient for RNA-binding protein brunol1 show reduction of spermatogenesis but are fertileMOLECULAR REPRODUCTION & DEVELOPMENT, Issue 11 2007Arvind Dev Abstract RNA-binding proteins are involved in post-transcriptional processes like mRNA stabilization, alternative splicing, and transport. Brunol1 is a novel mouse gene related to elav/Bruno family of genes encoding for RNA-binding proteins. We report here the expression and functional analysis of murine Brunol1. Expression analysis of Brunol1 during embryogenesis by RT-PCR showed that Brunol1 expression starts at 9.5 dpc and continues to the later stages of embryonic development. In adult mice, the Brunol1 expression is restricted to brain and testis. We also analyzed the Brunol1 expression in testes of different mutants with spermatogenesis defects: W/WV, Tfm/y, Leyl,/,, olt/olt, and qk/qk. Brunol1 transcript was detectable in Leyl,/,, olt/olt, and qk/qk mutant but not in W/WV and Tfm/y mutants. We also showed by transfection of a fusion protein of green fluorescent protein and Brunol1 protein into NIH3T3 cells, that Brunol1 is localized in cytoplasm and nucleus. In order to elucidate the function of the Brunol1 protein in spermatogenesis, we disrupted the Brunol1 locus in mouse by homologous recombination, which resulted in a complete loss of the Brunol1 transcript. Male and female Brunol1+/, and Brunol1,/, mice from genetic backgrounds C57BL/6J,×,129/Sv hybrid and 129X1/SvJ when inbred exhibited normal phenotype and are fertile, although the number and motility of sperms are significantly reduced. An intensive phenotypic analysis showed no gross abnormalities in testis morphology. Collectively our results demonstrate that Brunol1 might be nonessential protein for mouse embryonic development and spermatogenesis. Mol. Reprod. Dev. 74: 1456,1464, 2007. © 2007 Wiley-Liss, Inc. [source] Protein distribution of Kcnq1, Kcnh2, and Kcne3 potassium channel subunits during mouse embryonic developmentTHE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 3 2006Marķa Pilar de Castro Abstract Voltage-dependent potassium channels consist of a pore-forming ,-subunit, which is modulated by additional ,-ancillary or regulatory subunits. Kcnq1 and Kcnh2 ,-channel subunits play pivotal roles in the developing and adult heart. However, Kcnq1 and Kcnh2 have a much wider expression profile than strictly confined to the myocardium, similar to their putative regulatory Kcne1-5 ,-subunits. At present, the distribution of distinct potassium channel subunits has been partially mapped in adult tissues, whereas almost no information is available during embryonic development. In this study, we report a detailed analysis of Kcnq1, Kcnh2, and Kcne3 protein expression during mouse embryogenesis. Our results demonstrate that Kcnq1 and Kcnh2 are widely distributed. Coexpression of both ,-subunits is observed in a wide variety of organs, such as heart and the skeletal muscle, whereas others display unique Kcnq1 or Knch2 expression. Interestingly, Kcne3 expression is also widely observed in distinct tissue layers during embryogenesis, supporting the notion that an exquisite balance of ,- and ,-subunit expression is required for modulating potassium conductance in distinct organs and tissue layers. © 2006 Wiley-Liss, Inc. 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