RA-induced prominence-specific response resulted in distinctive regulation of Wnt and osteogenesis [miRNA-seq]
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE238063 | GEO | 2023/07/29
REPOSITORIES: GEO
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Project description:Proper retinoic acid (RA) signaling is essential for normal craniofacial development. Both excessive RA and RA deficiency in early embryonic stage led to a variety of craniofacial malformations, e.g., cleft palate, which have been investigated extensively. Dysregulated Wnt and Shh signaling were shown to underlie the pathogenesis of RA-induced craniofacial defects. In our present study, we showed a spatiotemporal-specific effect of RA signaling in regulating early development of facial prominences. While inhibited the Wnt activities in E12.5/E13.5 mouse palatal shelves, early exposure of excessive RA induced Wnt signaling and Wnt-related gene expression in mouse embryonic Frontonasal/Maxillary processes. A conserved regulatory network of miR-484-Fzd5 was identified to play critical roles in RA regulated craniofacial development using RNA-seq.
2023-07-29 | GSE238062 | GEO
Project description:We report the RNA profiles of both control and talpid2 frontonasal, maxillary, and mandibular prominences of the chick face at Hamburger and Hamilton (HH) stage 25. For more details please see: "The cellular and molecular etiology of the craniofacial defects in the avian ciliopathic mutant, talpid2." Facial prominences (frontonasal, maxillary, and mandibular) from 8 control and 8 talpid2 HH 25 embryos were harvested, pooled, and RNA-seq was preformed on samples.
2014-06-24 | E-GEOD-52757 | biostudies-arrayexpress
Project description:We report the RNA profiles of both control and talpid2 frontonasal, maxillary, and mandibular prominences of the chick face at Hamburger and Hamilton (HH) stage 25. For more details please see: "The cellular and molecular etiology of the craniofacial defects in the avian ciliopathic mutant, talpid2."
2014-06-24 | GSE52757 | GEO
Project description:Growth and patterning of the face relies on several small buds of tissue, the facial prominences, which surround the primitive mouth. Beginning around E10 of mouse development the prominences undergo rapid growth and morphogenesis. By E11.5 the medial nasal prominences are in close apposition in the midline, as are the maxillary and medial nasal prominences on either side of the developing face. Subsequently, by E12.5 the nasal and maxillary prominences fuse to form a continuous shelf at the front of the face - the primary palate. Individual prominences are associated with specific developmental processes, and this is reflected by patterns of differential gene expression that give the prominences their unique identities. Thus, only the mandibular and maxillary prominences give rise to dentition while the frontonasal prominence has a unique role in olfaction, and the mandibular prominence in taste. We used microarrays to detail the differential gene expression program in each of the mandibular, maxillary, and frontonasal prominences during the key developmental timepoints of E10.0 through E12.5. Keywords: time course
2008-08-30 | GSE7759 | GEO
Project description:Growth and patterning of the face relies on several small buds of tissue, the facial prominences, which surround the primitive mouth. Beginning around E10 of mouse development the prominences undergo rapid growth and morphogenesis. By E11.5 the medial nasal prominences are in close apposition in the midline, as are the maxillary and medial nasal prominences on either side of the developing face. Subsequently, by E12.5 the nasal and maxillary prominences fuse to form a continuous shelf at the front of the face - the primary palate. Individual prominences are associated with specific developmental processes, and this is reflected by patterns of differential gene expression that give the prominences their unique identities. Thus, only the mandibular and maxillary prominences give rise to dentition while the frontonasal prominence has a unique role in olfaction, and the mandibular prominence in taste. We used microarrays to detail the differential gene expression program in each of the mandibular, maxillary, and frontonasal prominences during the key developmental timepoints of E10.0 through E12.5. Experiment Overall Design: Analysis of gene expression during growth and fusion of the facial prominences in the C57BL/6J mouse strain between embryonic (E) day 10.0 and 12.5. At the earliest timepoint, E10, only the mandibular prominence is a distinct entity that can be readily identified and dissected. The frontonasal prominence and the maxillary prominence are very small and not discrete from other components of the head such as the forebrain until E10.5. Analysis of these tissues at earlier timepoints would require laser capture and preamplification steps - techniques that were not used for the later timepoints. Thus samples were isolated from the mandibular prominence at E10.0 and from the mandibular, maxillary and frontonasal prominences of mouse embryos from E10.5 to E12.5, at 0.5 day intervals. In order to obtain sufficient sample for hybridization, each sample represents a pool of between 3 and 48 embryos depending on the timepoint. Specifically, the number of embryos were 40-48 for E10.0 (mandibular prominence only), 24-8 for E10.5, 8-9 for E11.0 and E11.5 and 3-4 for E12.0 and E12.5. Seven replicate samples were taken for each of the later five timepoints in each of the three prominences, with an additional seven samples for the mandibular E10.0 timepoint, for a total of 112 samples.
2008-10-26 | E-GEOD-7759 | biostudies-arrayexpress
Project description:The face is one of the three regions most frequently affected by congenital defects in humans. In order to understand the molecular mechanisms involved it is necessary to have a more complete picture of gene expression in the embryo. Here we use microarrays to profile expression in chicken facial prominences, post neural crest migration and prior to differentiation of mesenchymal cells. Chip-wide analysis revealed that maxillary and mandibular prominences had similar expression profiles while the frontonasal mass chips were distinct. Of the 3094 genes that were differentially expressed in one or more regions of the face, a group of 56 genes was subsequently validated with quantitative PCR and a subset examined with in situ hybridization. Microarrays trends were consistent with the QPCR data for the majority of genes (81%). On the basis of QPCR and microarray data, groups of genes that characterize each of the facial prominences can be determined. We used microarrays to detail the global programme of gene expression underlying facial morphogensis keyword: craniofacial
2009-10-30 | GSE18477 | GEO
Project description:The rapid regeneration of the small intestinal epithelium is sustained by crypt intestinal stem cells (ISCs). Wnt/b-catenin signaling is essential for intestinal crypt homeostasis and maintenance of Lgr5+ ISC, and yet no single or combinatorial knockout of Frizzled (FZD) genes, representing Wnt receptors, has phenocopied the severe intestinal epithelial effects of Wnt signaling blockade. The elusive identification of specific Frizzled (Fzd) receptor(s) underlying homeostatic proliferation and ISC function would greatly inform therapeutic mucosal repair strategies. In prior pharmacologic studies, bioengineered antagonists that block Wnt binding to both FZD5 and FZD8 receptors induced lethal crypt and villus loss, implicating FZD5 and/or FZD8 as essential for ISCs maintenance. Here, the potential function of Fzd5 in during intestinal homeostasis was examined by epithelial-specific Fzd5 ko, which rapidly elicited lethal pan-intestinal crypt and villus loss, and by Lgr5-specific Fzd5 cKO, which strongly reduced Lgr5+ ISC while inducing their premature differentiation. In parallel, Fzd5 cKO potently repressed Wnt target gene expression, with phenotypic rescue by constitutive activation of b-catenin in vivo and confirmation upon in vitro organoid culture. Fzd5 cKO but not Fzd8 cKO in organoids ablated responsiveness to dual specificity bioengineered FZD5/FZD8-selective Wnt surrogate agonists, which reversed DSS-induced colitis phenotypes in both wild-type and Fzd8 cKO mice. Overall, our results implicate the FZD5 receptor as an essential regulator of crypt homeostasis, Lgr5+ ISCs and intestinal response to bioengineered Wnt surrogate agonists.
2024-10-18 | GSE233260 | GEO
Project description:The face is one of the three regions most frequently affected by congenital defects in humans. In order to understand the molecular mechanisms involved it is necessary to have a more complete picture of gene expression in the embryo. Here we use microarrays to profile expression in chicken facial prominences, post neural crest migration and prior to differentiation of mesenchymal cells. Chip-wide analysis revealed that maxillary and mandibular prominences had similar expression profiles while the frontonasal mass chips were distinct. Of the 3094 genes that were differentially expressed in one or more regions of the face, a group of 56 genes was subsequently validated with quantitative PCR and a subset examined with in situ hybridization. Microarrays trends were consistent with the QPCR data for the majority of genes (81%). On the basis of QPCR and microarray data, groups of genes that characterize each of the facial prominences can be determined. We used microarrays to detail the global programme of gene expression underlying facial morphogensis Experiment Overall Design: Chicken embryos were selected at a stage after neural crest cells have ceased migration, when facial prominences have formed and prior to ctyodifferentiation of cartilage, bone, muscle. Microdissection was used to isolate facial prominences. Embryos were dissected on ice in Hanks Buffered Salt Solution and batches of 26-32 pieces were snap frozen in liquid Nitrogen. These pooled facial prominences comprised one biological replicate. A total of three biological replicates were generated for the frontonasal mass, maxillary and mandibular prominences.
2009-11-10 | E-GEOD-18477 | biostudies-arrayexpress
Project description:We previously showed that the combination of markers LNGFR+ and THY-1+ can be used selectively to isolate human mesenchymal stem cells (hMSCs) in bone marrow and several tissues. However, the molecular mechanisms regulating stemness of hMSCs remain to be elucidated. In this study, we found that Frizzled 5 (FZD5) and Receptor tyrosine kinase-like orphan receptor 2 (ROR2) were highly enriched in LNGFR+THY-1+ derived clones that retain a high potential for proliferation (rapidly expanding clones; RECs). WNT5A, the ligand of FZD5, causes FZD5 and ROR2 to co-localize and activates non-canonical Wnt pathway in RECs. Moreover, FZD5 knockdown attenuated proliferation and caused senescence. In contrast, FZD5 overexpression delayed senescence. These results indicate that intrinsic activation of non-canonical Wnt signaling via FZD5 and ROR2 modulates stemness and senescence of RECs. Thus, control of non-canonical Wnt signaling would enable us to regulate hMSC quality and to enhance the efficacy of cell-replacement therapy using hMSCs.
2016-09-02 | GSE86369 | GEO
Project description:Wnt ligands oligomerize Frizzled (Fzd) and Lrp5/6 receptors to control the specification and activity of stem cells in many species. How Wnt is selectively activated in different stem cell populations, often within the same organ, is not understood. In lung alveoli, wherein Wnt-dependent epithelial and stromal progenitors are intermingled, we show that distinct Wnt receptors are expressed by epithelial (Fzd5/6), endothelial (Fzd4), and stromal (Fzd1) cells. Moreover, Fzd5 was uniquely required for alveolar epithelial stem cell activity. However, by developing an expanded repertoire of Fzd-Lrp agonists (FLAgs), we could activate canonical Wnt signaling in alveolar epithelial stem cells via either Fzd5 or, unexpectedly, non-canonical Fzd6. Fzd5 and Fzd6 FLAgs stimulated supra-physiological alveolar epithelial stem cell activity in mice following lung injury, but only Fzd6 FLAg promoted an alveolar fate in airway-derived progenitors. Therefore, we identify a potential strategy for promoting regeneration without exacerbating fibrosis during lung injury.
2023-06-16 | GSE208770 | GEO