Time-course of genes expression of the dorsal and lateral lineage in the SVZ-RMS-OB post-natal neurogenic system
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE69693 | GEO | 2017/06/28
SECONDARY ACCESSION(S): PRJNA286209
REPOSITORIES: GEO
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Project description:The adult subventricular zone (SVZ) is a highly organized microenvironment established during the first postnatal days when radial glia cells begin to transform into type B-cells and ependymal cells, all of which will form regenerative units, pinwheels, along the lateral wall of the lateral ventricle. Here, we identify p73, a p53 homologue, as a critical factor controlling both cell-type specification and structural organization of the developing mouse SVZ. We describe that p73 deficiency halts the transition of the radial glia into ependymal cells, leading to the emergence of immature cells with abnormal identities in the ventricle and resulting in loss of the ventricular integrity. p73-deficient ependymal cells have noticeably impaired ciliogenesis and they fail to organize into pinwheels, disrupting SVZ niche structure and function. Therefore, p73 is essential for appropriate ependymal cell maturation and the establishment of the neurogenic niche architecture. Accordingly, lack of p73 results in impaired neurogenesis. Moreover, p73 is required for translational planar cell polarity establishment, since p73 deficiency results in profound defects in cilia organization in individual cells and in intercellular patch orientation. Thus, our data reveal a completely new function of p73, independent of p53, in the neurogenic architecture of the SVZ of rodent brain and in the establishment of ependymal planar cell polarity with important implications in neurogenesis. © 2015 Wiley Periodicals, Inc. Develop Neurobiol 76: 730-747, 2016.
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Project description:Transcription factors of the nuclear factor one (NFI) family play a pivotal role in the development of the nervous system. One member, NFIX, regulates the development of the neocortex, hippocampus, and cerebellum. Postnatal Nfix(-/-) mice also display abnormalities within the subventricular zone (SVZ) lining the lateral ventricles, a region of the brain comprising a neurogenic niche that provides ongoing neurogenesis throughout life. Specifically, Nfix(-/-) mice exhibit more PAX6-expressing progenitor cells within the SVZ. However, the mechanism underlying the development of this phenotype remains undefined. Here, we reveal that NFIX contributes to multiple facets of SVZ development. Postnatal Nfix(-/-) mice exhibit increased levels of proliferation within the SVZ, both in vivo and in vitro as assessed by a neurosphere assay. Furthermore, we show that the migration of SVZ-derived neuroblasts to the olfactory bulb is impaired, and that the olfactory bulbs of postnatal Nfix(-/-) mice are smaller. We also demonstrate that gliogenesis within the rostral migratory stream is delayed in the absence of Nfix, and reveal that Gdnf (glial-derived neurotrophic factor), a known attractant for SVZ-derived neuroblasts, is a target for transcriptional activation by NFIX. Collectively, these findings suggest that NFIX regulates both proliferation and migration during the development of the SVZ neurogenic niche.
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Project description:In the present project we examined the effects of maternal obesity to offspring hypothalamic tissue at postnatal day (P) 21. Maternal obesity has emerged as an important risk factor for the development of metabolic disorders in the offspring.To obtain an overview of affected genes in the offsprings hypothalamus, the center of hunger and satiety in the brain, we performed whole genome microarray expression profiling. Female mice were fed either a control diet (SD) or a high fat diet (HFD) after weaning until mating and during pregnancy and gestation. On P21, male pups were sacrificed and blood samples were collected for further analyses. The hypothalamus was cut immediately caudal to the optic chiasm. The dissection was limited laterally by the hypothalamic sulci and dorsally by the mammillothalamic tract. Hypothalamic tissue was immediately frozen at −80° C. A maximum of two offspring per dam were analysed to minimize litter-dependent bias. All studies were performed using male offspring.
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Project description:Using RNA sequencing, this study aims to identify (1) downstream targets and (2) cellular processes depending on the transcription factor Zeb2 in the young postnatal neurogenic V-SVZ niche of the mouse brain
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Project description:Partial reprogramming has the potential to reverse age-related decline in some tissues. Its impact on the cell types within the aging brain, particularly the subventricular zone neurogenic niche, is unknown.
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Project description:The functional importance of oligodendrocyte developmental heterogeneity is unknown. Using a genetic strategy to ablate dorsally-derived oligodendrocyte lineage cells (OLCs), we found that the areas in which dorsally-derived OLCs normally reside in the adult CNS become populated and myelinated by OLCs of ventral origin. These ectopic oligodendrocytes (eOLs) have a distinctive gene expression profile, as well as subtle myelination abnormalities. The failure of eOLs to assume the role of the original dorsally-derived cells result in locomotor and cognitive deficits in the adult animal. This study reveals the importance of developmental heterogeneity within the oligodendrocyte lineage, and its importance for homeostatic brain function.
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Project description:We performed large-scale single cell profiling of dissociated V-SVZ and OB cells from the same animal carrying either the hGFAP::CreERT2; Rosa26LSL-TdTomato (GCERT2) reporter, or ratNes::FLPOER; Rosa26FSF-TdTomato (NesFLPO) reporter. Scope-Seq profiling was performed on dissociated V-SVZ cells from C57BL/6J animals.
2020-06-21 | GSE134918 | GEO
Project description:The sensory processing of odorants is a dynamic process that requires plasticity at multiple levels. In the olfactory bulb (OB), inhibitory interneurons undergo lifelong replacement through a process known as adult neurogenesis. These newly born cells are incorporated in a learning-dependent fashion, a process which has led some to suggest this as a primary mechanism through which the OB retains a high degree of plasticity throughout life. A continued focus of researchers in this field has been to understand the molecular mechanisms controlling adult subventricular zone (SVZ) neurogenesis and the innate functional role of these cells. Brain-derived neurotrophic factor (BDNF) has been identified as a strong candidate molecule regulating adult OB neurogenesis. We review what is known regarding the functional role of newly born cells, highlight the role of BDNF in this process, and describe preliminary findings from our lab implicating BDNF in the process of selecting of newly born cells for survival.
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Project description:A wide variety of microbial species, including Trichophyton spp., have been detected in diabetic foot ulcers (DFUs). In particular, Trichophyton spp. cause tinea pedis (i.e., athlete's foot) and onychomycosis. However, investigations regarding the correlation between Trichophyton spp. and delayed wound healing are limited to case reports. Moreover, histological changes in wounds caused by Trichophyton spp. remain unclear. In this study, we sought to confirm the delayed wound healing phenotype caused by Trichophyton mentagrophytes infection in a full-thickness excisional wound ob/ob mouse model through histopathological analysis. The inoculation of skin wounds in ob/ob mice with T. mentagrophytes sporules resulted in significant delay on wound healing. Further histopathological analyses demonstrated that the delayed wound healing in ob/ob mice was accompanied by reduced collagen fibre formation and inhibited granulation tissue formation, with spores and elongated mycelia retained in the wound bed and along the wound edges. This suggests that T. mentagrophytes colonization of wounds potentially contributes to delayed wound healing in patients with diabetes. These results suggest that neglected tinea pedis is a potential risk factor for delayed wound healing and progression to refractory wounds in patients with DFU.
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Project description:ObjectiveObesity increases morbidity and resource utilization in sepsis patients. Sepsis transitions from early/hyper-inflammatory to late/hypo-inflammatory phase. Majority of sepsis-mortality occurs during the late sepsis; no therapies exist to treat late sepsis. In lean mice, we have shown that sirtuins (SIRTs) modulate this transition. Here, we investigated the role of sirtuins, especially the adipose-tissue abundant SIRT-2 on transition from early to late sepsis in obese with sepsis.MethodsSepsis was induced using cecal ligation and puncture (CLP) in ob/ob mice. We measured microvascular inflammation in response to lipopolysaccharide/normal saline re-stimulation as a "second-hit" (marker of immune function) at different time points to track phases of sepsis in ob/ob mice. We determined SIRT-2 expression during different phases of sepsis. We studied the effect of SIRT-2 inhibition during the hypo-inflammatory phase on immune function and 7-day survival. We used a RAW264.7 (RAW) cell model of sepsis for mechanistic studies. We confirmed key findings in diet induced obese (DIO) mice with sepsis.ResultsWe observed that the ob/ob-septic mice showed an enhanced early inflammation and a persistent and prolonged hypo-inflammatory phase when compared to WT mice. Unlike WT mice that showed increased SIRT1 expression, we found that SIRT2 levels were increased in ob/ob mice during hypo-inflammation. SIRT-2 inhibition in ob/ob mice during the hypo-inflammatory phase of sepsis reversed the repressed microvascular inflammation in vivo via activation of endothelial cells and circulating leukocytes and significantly improved survival. We confirmed the key finding of the role of SIRT2 during hypo-inflammatory phase of sepsis in this project in DIO-sepsis mice. Mechanistically, in the sepsis cell model, SIRT-2 expression modulated inflammatory response by deacetylation of NFκBp65.ConclusionSIRT-2 regulates microvascular inflammation in obese mice with sepsis and may provide a novel treatment target for obesity with sepsis.
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