Gene expression profiles in mouse embryonic midbrain of Wnt1-lineage specific Gpr161 deletion.
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ABSTRACT:
PROVIDER: PRJNA768779 | ENA |
REPOSITORIES: ENA
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Project description:To explore the differentially expressed genes in embryonic midbrain development in Wnt1-lineage specific Gpr161 deleted mouse embryos.
2021-12-15 | GSE185336 | GEO
Project description: Not available
| S-EPMC8650154 | biostudies-literature
Project description:The development of the mesodiencephalic dopaminergic (mdDA) neurons strongly depends on the WNT1/b-catenin signaling pathway. These neurons include the Substantia nigra pars compacta (SNc) subset that preferentially degenerates in Parkinson’s Disease (PD), and the ventral tegmental area (VTA) subpopulation implicated in a variety of neuropsychiatric disorders. The identity of the cells responding to this signaling pathway in the developing mammalian ventral midbrain (VM) and the precise mechanism of WNT/b-catenin action in these cells, however, are still unknown. Moreover, this signaling pathway has to be accurately balanced during mdDA neuron development: whereas low levels or absence of WNT1/b-catenin signaling abolish their correct specification, constitutive activation of this signaling pathway prevents their proper differentiation in the mouse. We show that the WNT/b-catenin-responsive cells constitute only a fraction of all mdDA progenitors, precursors and neurons in the murine VM. These WNT/b-catenin-responsive cells are mostly located in the Wnt1+, Rspo2+ and Lef1+ lateral floor plate of the medial and caudal midbrain, giving preferentially rise to caudomedial (VTA) mdDA neurons. Strong WNT/b-catenin signaling mediated by RSPO2, a WNT/b-catenin agonist, and LEF1, a nuclear effector of this pathway, inhibits the differentiation of WNT/b-catenin-responsive mdDA progenitors into mature mdDA neurons by repressing the murine Pitx3 gene via conserved LEF1/TCF binding sites in its promoter. Our data indicate that an attenuation of WNT/b-catenin signaling in mdDA progenitors is essential for their correct differentiation into specific mdDA neuron subsets, thus providing a new means for stem cell-based regenerative therapies of PD and in vitro models of neuropsychiatric diseases.
2020-09-02 | GSE99618 | GEO
Project description:We hypothesized that CD44+ tumor cells might have an increased capacity for reactive oxygen species (ROS) defense in the gastric tumors of K19-Wnt1/C2mE mice. To address this possibility, we examined the expression of antioxidant genes in tumor cells isolated from K19-Wnt1/C2mE mice by fluorescence-activated cell sorting (FACS). Lineage marker (Lin)–negative cells that were CD44+ or CD44– were thus isolated from the gastric tumors of 30-week-old K19-Wnt1/C2mE mice and subjected to cDNA microarray analysis. The expression of several key antioxidant genes, including those for glutathione peroxidase (GPX) and peroxiredoxin (PRDX) isoforms, was found to be increased in CD44+ tumor cells compared with that in CD44– cells.
2010-03-17 | GSE20913 | GEO
Project description:Previously we have demonstrated that inactivation of retinoic acid receptor beta (Rarb) in the mouse results in a protective effect against ErbB2-induced mammary gland tumorigenesis although Rarb has been reported as a tumor suppressor before. In the current study, we further confirmed that ablation of Rarb has a very similar impact on Wnt1-induced mammary gland tumorigenesis as those on ErbB2-induced mammary gland tumorigenesis. Nevertheless, the mechanisms by which Rarb confers its effects on tumor progression is quite different although both involving in tumor microenvironment (TME) remodeling. In the Wnt1 tumors, ectopic wnt1 produced by malignant luminal cells activates nearby stromal cells by a paracrine manner. In return, the stromal cells secreted IGF1 to regulate the growth of tumor cells. There is a need of Rarb expression in this interaction. Deletion of Rarb inhibits both wnt1/β-catenin signaling and IGF1/Akt axis in the myoepithelial tumor cells which results in the suppression of epithelial-mesenchymal transition (EMT) in these tumors. Since wnt1 tumors resemble basal-like breast cancer with a poor clinical prognosis in which EMT is one of the most important way for tumor cells to survive against standard treatment and to go to metastasis, we propose that (1) the stromal gene expression signature of Rarb ablation in wnt1 tumors could have some clinical value in predicting the breast cancer outcome; and (2) Rarb antagonist might be a potential therapeutic strategy in EMT-driven aggressive cancers such as basal-like breast cancer. Laser capture microdissection (LCM) was performed to separate the mammary tumor samples into epithelial cell compartment and stromal cell compartment. Transcriptional profiling of the two compartments were investigated by microarray analysis.
2014-10-23 | E-GEOD-56391 | biostudies-arrayexpress
Project description:Wnt1 has major anabolic functions in bone metabolism. We investigated the effect of recombinant murine Wnt1/Sfrp1 complex on the mesenchymal cell line ST2. We used microarray analysis to detail the global gene expression of ST2 cells in response to 6 hour of treatment with 100 ng recombinant Wnt1/Sfrp1 complex.
2022-08-17 | GSE211391 | GEO
Project description:bulk RNA-seq of wild-type, Gli2f/f;Gli3f/f;Wnt1-Cre, and Hand2f/f;Wnt1-Cre mouse e10.5 dissection mandibular prominences
2020-10-01 | GSE141431 | GEO
Project description:Previously we have demonstrated that inactivation of retinoic acid receptor beta (Rarb) in the mouse results in a protective effect against ErbB2-induced mammary gland tumorigenesis although Rarb has been reported as a tumor suppressor before. In the current study, we further confirmed that ablation of Rarb has a very similar impact on Wnt1-induced mammary gland tumorigenesis as those on ErbB2-induced mammary gland tumorigenesis. Nevertheless, the mechanisms by which Rarb confers its effects on tumor progression is quite different although both involving in tumor microenvironment (TME) remodeling. In the Wnt1 tumors, ectopic wnt1 produced by malignant luminal cells activates nearby stromal cells by a paracrine manner. In return, the stromal cells secreted IGF1 to regulate the growth of tumor cells. There is a need of Rarb expression in this interaction. Deletion of Rarb inhibits both wnt1/β-catenin signaling and IGF1/Akt axis in the myoepithelial tumor cells which results in the suppression of epithelial-mesenchymal transition (EMT) in these tumors. Since wnt1 tumors resemble basal-like breast cancer with a poor clinical prognosis in which EMT is one of the most important way for tumor cells to survive against standard treatment and to go to metastasis, we propose that (1) the stromal gene expression signature of Rarb ablation in wnt1 tumors could have some clinical value in predicting the breast cancer outcome; and (2) Rarb antagonist might be a potential therapeutic strategy in EMT-driven aggressive cancers such as basal-like breast cancer.
2014-10-23 | GSE56391 | GEO
Project description:Embryonic stem (ES) cells were differentiated in culture to midbrain dopaminergic (mDA) progenitors and subjected to ChIP-seq analysis to resolve genome-wide binding sites of forkhead box protein A2 (Foxa2). Foxa2 was found to directly regulate multiple lineage pathways to specify midbrain dopaminergic and floor plate progenitor identity.
2012-07-01 | E-MTAB-1137 | biostudies-arrayexpress
Project description:To improve the standardization of cell therapies for Parkinson’s disease, methods for the selection and isolation of midbrain dopaminergic progenitors for transplantation are required. To facilitate this we established an expression profile for genes selectively expressed on transplantable midbrain dopaminergic progenitors using microarray analysis.
2015-02-28 | GSE65094 | GEO