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10.1371/journal.pone.0197356 http://scihub22266oqcxt.onion/10.1371/journal.pone.0197356 C5957351!5957351 !29771971     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=29771971 &cmd=llinks): Failed to open stream: HTTP request failed! 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Constitutive metanephric mesenchyme-specific expression of interferon-gamma causes renal dysplasia by regulating Sall1 expression |pdf=|usr=}}{{29771971 }} gab.com Text Constitutive metanephric mesenchyme-specific expression of interferon-gamma causes renal dysplasia by regulating Sall1 expression JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29771971 #FOAvip Transplacental viral and parasitic infections have been shown to initiate an innate response in the mammalian embryo by increasing the expression of pro-inflammatory cytokines such as interferon-gamma (Ifng). However, the developmental consequences of an activated innate immunity and, in particular, the effects of induction of Ifng expression independent of infection have been largely overlooked. Here, we demonstrate in vivo that the conditional overexpression of Ifng in metanephric mesenchymal (MM) progenitors results in renal agenesis or hypoplasia. Cell death was observed in and around the MM region of E10.5-11.5 mutants where Ifng was constitutively expressed during early kidney development and resulted in a retardation of branching morphogenesis. Furthermore, isolated mutant or normal Ifng-treated metanephroi replicated this phenotype in culture, demonstrating the inherent nature of the aberrant morphogenesis. The expression of renal progenitor marker Sall1 was significantly decreased in the MM of mutant kidneys, suggesting that a reduction in Sall1 may be the cause of cell death in the MM during early kidney development and that, in turn, retards UB branching in the mutants. Therefore, the aberrant induction of Ifng expression, as part of an innate immune response, may contribute to renal agenesis or hypoplasia during early metanephric development by regulating the MM progenitor population. Twit Text FOAVip Constitutive metanephric mesenchyme-specific expression of interferon-gamma causes renal dysplasia by regulating Sall1 expression ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=29771971 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29771971 #FOAvip English Wikipedia <ref>{{Cite pmid|29771971 }}</ref> Constitutive metanephric mesenchyme-specific expression of interferon-gamma causes renal dysplasia by regulating Sall1 expression #MMPMID29771971 Yun K ; Hurwitz AA ; Perantoni AO PLoS One 2018[]; 13 (5 ): e0197356 PMID29771971 show ga Transplacental viral and parasitic infections have been shown to initiate an innate response in the mammalian embryo by increasing the expression of pro-inflammatory cytokines such as interferon-gamma (Ifng). However, the developmental consequences of an activated innate immunity and, in particular, the effects of induction of Ifng expression independent of infection have been largely overlooked. Here, we demonstrate in vivo that the conditional overexpression of Ifng in metanephric mesenchymal (MM) progenitors results in renal agenesis or hypoplasia. Cell death was observed in and around the MM region of E10.5-11.5 mutants where Ifng was constitutively expressed during early kidney development and resulted in a retardation of branching morphogenesis. Furthermore, isolated mutant or normal Ifng-treated metanephroi replicated this phenotype in culture, demonstrating the inherent nature of the aberrant morphogenesis. The expression of renal progenitor marker Sall1 was significantly decreased in the MM of mutant kidneys, suggesting that a reduction in Sall1 may be the cause of cell death in the MM during early kidney development and that, in turn, retards UB branching in the mutants. Therefore, the aberrant induction of Ifng expression, as part of an innate immune response, may contribute to renal agenesis or hypoplasia during early metanephric development by regulating the MM progenitor population. |Animals [MESH] |Cell Death/physiology [MESH] |Gene Expression Regulation, Developmental [MESH] |Interferon-gamma/genetics/*metabolism [MESH] |Kidney/*abnormalities/*embryology/metabolism [MESH] |Mesenchymal Stem Cells/*metabolism [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Organogenesis/physiology [MESH] |Tissue Culture Techniques [MESH]Constitutive metanephric mesenchyme-specific expression of interferon-(epmc).pdf DeepDyve Pubget Overpricing