Developmental dynamics : an official publication of the American Association of Anatomists · 2023
β-Catenin in the kidney stroma modulates pathways and genes to regulate kidney development.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Deacon Erin, Li Anna, Boivin Felix, Dvorkin-Gheva Anna, Cunanan Joanna, Bridgewater Darren
Аннотация
BACKGROUND: Kidney development is regulated by cellular interactions between the ureteric epithelium, mesenchyme, and stroma. Previous studies demonstrate essential roles for stromal β-catenin in kidney development. However, how stromal β-catenin regulates kidney development is not known. We hypothesize that stromal β-catenin modulates pathways and genes that facilitate communications with neighboring cell populations to regulate kidney development.
RESULTS: We isolated purified stromal cells with wild type, deficient, and overexpressed β-catenin by fluorescence-activated cell sorting and conducted RNA Sequencing. A Gene Ontology network analysis demonstrated that stromal β-catenin modulates key kidney developmental processes, including branching morphogenesis, nephrogenesis and vascular formation. Specific stromal β-catenin candidate target genes that may mediate these effects included secreted, cell-surface and transcriptional factors that regulate branching morphogenesis and nephrogenesis (Wnts, Bmp, Fgfr, Tcf/Lef) and secreted vascular guidance cues (Angpt1, VEGF, Sema3a). We validated established β-catenin targets including Lef1 and novel candidate β-catenin targets including Sema3e which have unknown roles in kidney development.
CONCLUSIONS: These studies advance our understanding of gene and biological pathway dysregulation in the context of stromal β-catenin misexpression during kidney development. Our findings suggest that during normal kidney development, stromal β-catenin may regulate secreted and cell-surface proteins to communicate with adjacent cell populations.
RESULTS: We isolated purified stromal cells with wild type, deficient, and overexpressed β-catenin by fluorescence-activated cell sorting and conducted RNA Sequencing. A Gene Ontology network analysis demonstrated that stromal β-catenin modulates key kidney developmental processes, including branching morphogenesis, nephrogenesis and vascular formation. Specific stromal β-catenin candidate target genes that may mediate these effects included secreted, cell-surface and transcriptional factors that regulate branching morphogenesis and nephrogenesis (Wnts, Bmp, Fgfr, Tcf/Lef) and secreted vascular guidance cues (Angpt1, VEGF, Sema3a). We validated established β-catenin targets including Lef1 and novel candidate β-catenin targets including Sema3e which have unknown roles in kidney development.
CONCLUSIONS: These studies advance our understanding of gene and biological pathway dysregulation in the context of stromal β-catenin misexpression during kidney development. Our findings suggest that during normal kidney development, stromal β-catenin may regulate secreted and cell-surface proteins to communicate with adjacent cell populations.