Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA122805 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series:; GSE16691: Transcriptional regulation by Norrin-Frizzled4 signaling in the embryonic yolk sac; GSE16703: Long-term effect on the transcriptome of a decrement in Norrin/Frizzled4/Lrp signaling in retinal endothelial cells; GSE16705: Transcriptional response to Frizzled4 signaling in cultured retinal endothelial cells; GSE16707: Long-term effect on the transcriptome of loss of Frizzled4 signaling in cerebellar endothelial cells Experiment Overall Design: Refer to individual Series
2009-10-10 | E-GEOD-16841 | biostudies-arrayexpress
Project description:Long-term effect on the transcriptome of a decrement in Norrin/Frizzled4/Lrp signaling in retinal endothelial cells
| PRJNA122803 | ENA
Project description:Transcriptional profiles of Fz4-/- retinal endothelial cells were compared to that of wild type endothelial cells under various culture conditions. The goal was to identify the transcriptional response to Frizzled 4 signaling in cultured retinal endothelial cells. To analyze the Norrin response of WT and Fz4-/- retinal endothelial cells in culture, we co-cultured these cells either with HEK293 cell line that stably expresses Norrin or with control 293 cells.
2009-10-01 | GSE16705 | GEO
Project description:Long-term effect on the transcriptome of loss of Frizzled4 signaling in cerebellar endothelial cells
| PRJNA122687 | ENA
Project description:In mammals, retinal damage is followed by Müller glia cell activation and proliferation. While retinal gliosis persists in adult mammals after an insult or disease, some vertebrates, including zebrafish, have the capacity to regenerate. We believe we are the first group to show that gliosis is a fibrotic-like process in mammals’ eyes caused by differential activation of canonical and non-canonical TGFβ signaling pathways.
2019-11-03 | GSE132140 | GEO
Project description:Transcriptional regulation by Norrin-Frizzled4 signaling in the embryonic yolk sac
| PRJNA122703 | ENA
Project description:Transcriptional profiles of Fz4-/- retinal endothelial cells were compared to that of wild type endothelial cells under various culture conditions. The goal was to identify the transcriptional response to Frizzled 4 signaling in cultured retinal endothelial cells. To analyze the Norrin response of WT and Fz4-/- retinal endothelial cells in culture, we co-cultured these cells either with HEK293 cell line that stably expresses Norrin or with control 293 cells. Experiment Overall Design: To isolate the requisite retinal endothelial cell lines, we crossed Fz4-/- and control animals into the Immorto-mouse line in which a gamma interferon responsive H2Kb promoter directs the expression of a temperature sensitive SV40 large T-antigen (Jat et al., 1991). When cultured at 33°C in the presence of gamma interferon, this conditional oncogene system extends the proliferative capacity of a variety of cell types, which can be subsequently analyzed under phenotypically reverting conditions (37°C without gamma interferon). The cell immuno-purification procedure follows that described by Matsubara et al. (2000) and Su et al. (2003). The purified cells were then cultured and passaged at 33°C on dishes coated with 1% gelatin. For RNA preparation, cells were cultured at 37°C in the absence of interferon gamma. For the Matrigel experiments, endothelial cells previously starved for 24 hrs in DMEM with 1% FBS were trypsinized and plated on the Matrigel layer. The cells were incubated in DMEM with 1% FBS for 6 hours at 37°C before harvesting for RNA extraction. For the 293 cell co-culture experiments, endothelial cells were co-cultured with a human embryonic kidney (HEK) 293 cell line that stably expresses Norrin, or with control 293 cells.
2009-10-10 | E-GEOD-16705 | biostudies-arrayexpress
Project description:Using mice with targeted gene mutations, we identify (1) distinct roles for different canonical Wnt signaling components in central nervous system (CNS) vascular development and in the specification of the blood-brain and blood-retina barriers (BBB and BRB) and (2) differential sensitivities of the vasculature in various CNS regions to perturbations in canonical Wnt signaling components. We find nearly equivalent roles for Lrp5 and Lrp6 in brain vascular development and barrier maintenance but a dominant role for Lrp5 in the retinal vasculature, an especially high sensitivity of the BBB in the cerebellum and pons/interpeduncular nuclei to decrements in canonical Wnt signaling, and plasticity in the barrier properties of mature CNS vasculature. Brain and retinal vascular defects caused by loss of Norrin/Frizzled4 signaling can be fully rescued by stabilizing beta-catenin, and loss of beta-catenin’s transcriptional activation domain or expression of a dominant negative Tcf4 recapitulates the vascular development and barrier defects seen with loss of receptor, co-receptor, or ligand, indicating that Norrin/Frizzled4 signaling acts predominantly by beta-catenin-dependent transcriptional regulation. This work strongly supports a model in which identical or nearly identical canonical Wnt signaling mechanisms mediate neural tube and retinal vascularization and maintain the BBB and BRB. Total retina RNA from P10 WT, NdpKO, Ctnnb1flex3/+;Pdgfb-CreER, and NdpKO;Ctnnb1flex3/+;Pdgfb-CreER mice was subjected to RNAseq
2014-06-05 | E-GEOD-56461 | biostudies-arrayexpress
Project description: Not available
| S-EPMC8784167 | biostudies-literature
Project description:The retinal transcriptional response to light damage
| PRJNA108943 | ENA