Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA291057 | ENA |
REPOSITORIES: ENA
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Project description:Myelination calls for a tremendous surge in cell metabolism towards lipids and membrane production. However, functional relevance of de novo fatty acid synthesis in myelinating cells remains unclear. We generated mutant mice in which the enzyme fatty acid synthase (FASN) was depleted conditionally in Schwann cells, the myelinating glial cells of the peripheral nervous system. To address how lack of FASN was affecting the development of the peripheral nervous system, we screened with an Affymetrix Transcriptomic approach the transcriptome of sciatic nerves and roots of P60 FASN mutant mice, comparing to control mice.
2018-02-02 | GSE71373 | GEO
Project description:Transcriptional Profiling of Neuronal APP/APLP2 Double-Conditional Knockout Mice.
2015-07-16 | E-GEOD-48622 | ExpressionAtlas
Project description:RNA sequencing (RNA-SEQ) of Dnmt1 and Dnmt3a conditional knockout mice
2019-05-14 | E-GEOD-58261 | ExpressionAtlas
Project description:Gene expression profile of retina and pineal gland of NeuroD1 conditional knockout mice
2015-09-22 | E-GEOD-35396 | ExpressionAtlas
Project description:Formation of myelin by Schwann cells is tightly coupled to peripheral nervous system development and is important for neuronal function and long-term maintenance. Perturbation of myelin causes a number of specific disorders that are among the most prevalent diseases affecting the nervous system. Schwann cells synthesize myelin lipids de novo rather than relying on uptake of circulating lipids, yet one unresolved matter is how Acetyl CoA, a central metabolite in lipid formation is generated during myelin formation and maintenance. Recent studies have shown that glucose-derived Acetyl CoA itself is not required for myelination. Moreover, the importance of mitochondrially-derived Acetyl CoA has never been tested for myelination in vivo. Therefore, we have developed a Schwann cell-specific knockout of the ATP Citrate Lyase (Acly) gene to determine the importance of mitochondrial metabolism to supply Acetyl CoA in nerve development. Intriguingly, the ACLY pathway is important for myelin maintenance rather than myelin formation. In addition, ACLY is required to maintain expression of a myelin-associated gene program and to inhibit activation of the latent Schwann cell injury program.
2024-03-25 | MSV000094403 | MassIVE
Project description:The aim of our study is to determine the functions of histone deacetylases (HDACs) 1 and 2 in Schwann cells during postnatal development of the peripheral nervous system (PNS). Schwann cells are the myelinating glial cells of the PNS. At birth, mouse sciatic nerves mature in 2 subsequent phases: 1/ big caliber axons get sorted into a 1 to 1 relationship with Schwann cells, 2/ Schwann cells build a myelin sheath around sorted axons. In mice where both HDAC1 & HDAC2 have been specifically knocked out in Schwann cells, both phases are impaired. HDACs are chromatin remodeling enzymes, they can thus alter gene expression directly. We want to identify which genes controlled by HDAC1 and HDAC2 in Schwann cells are necessary for the maturation of sciatic nerves. Because HDAC1 and HDAC2 can compensate for each other loss to some extend, we will first analyze changes of gene expression in HDAC1/HDAC2 double KO animals. We expect to gain critical insights into the molecular mechanisms controlling Schwann cell differentiation and myelination. This knowledge is of key importance for the success of regenerative medicine in peripheral neuropathies, nerve tumors, and transplantation paradigms in non-regenerative CNS lesions and in large PNS injuries. 3 double knockout mutants for HDAC1 and HDAC2 and 3 control littermates were analyzed. Tissues analyzed: sciatic nerves of 2 day-old mouse pups
2011-02-25 | E-GEOD-27451 | biostudies-arrayexpress
Project description:Neural stem cells (NSCs) are most commonly sourced from neural tissue such as the central nervous system or the enteric nervous system (ENS) of the gut. Emerging evidence has shown that adipose tissue contains its own complex nervous system consisting of sympathetic and sensory innervation. The entirety of the peripheral nervous system is the progeny of Wnt1-expressing cells of the embryonic neural crest. This includes the ENS, autonomic neurons, and Schwann cell precursors that provide peripheral glial cells. Counterintuitive to their name, however, embryonic Schwann cell precursors represent multipotent stem cells that migrate along embryonic nerve fibers and contribute to glial and non-glial cell populations, including melanocytes, neuroendocrine chromaffin cells, enteric neurons, sympathetic neurons and mesenchymal stem cells from the bone marrow, depending on local environmental cues. However, no equivalent progenitors are known to exist postnatally in the nerve fiber niche. Schwann cells have been demonstrated to give rise to enteric neurons postnatally, suggesting they retain neuronal progenitor properties and offer a potential source of NSCs for regenerative therapies. In this study, we compare the transcriptomic properties of neural crest-derived NSCs from the intestine (enteric neural progenitors) and the nerve fibers of the subcutaneous adipose tissue and evaluate the effects of different methods of NSC culture and isolation.
2022-05-31 | GSE200689 | GEO
Project description:During peripheral nervous system (PNS) development, Schwann cells (SC) depend on interactions between extracellular matrix proteins, integrins and growth factor signal transduction pathways for survival, sorting and wrapping of axon segments to form myelin. Together with integrin-linked-kinase and parvins, PINCH (Particularly-interesting-new-cystidin-hystidin-rich protein) forms a heterotrimeric complex referred to as the IPP complex, which functions as a signaling hub connecting integrins with various signaling pathways. Using SC-specific conditional gene targeting in mice, gene expression profiling by RNAseq, and other methodologies, we demonstrate distinct functional roles for PINCH1 and PINCH2 in SC.
2017-12-31 | GSE106413 | GEO
Project description:Peripheral nerves contain axons and their enwrapping glia cells named Schwann cells (SC) that are either myelinating or non-myelinating (nmSC). Our understanding of other cells in the peripheral nervous system (PNS) remains limited. Here, we provide an unbiased single-cell transcriptomic characterization of the non-diseased rodent PNS. We identified and independently confirmed novel markers of previously underappreciated nmSC and nerve-associated fibroblasts. We also found and characterized two distinct populations of nerve-resident homeostatic myeloid cells that transcriptionally differed from central nervous system microglia. In a model of chronic autoimmune neuritis, homeostatic myeloid cells were outnumbered by infiltrating lymphocytes which modulated the local cell-cell interactome and induced a specific transcriptional response in glia cells. This response was partially shared between the peripheral and central nervous system glia identifying common immunological features across different parts of the nervous system. Our study thus identifies novel subtypes and cell-type markers of PNS cells and a partially conserved autoimmunity module induced in glia cells.
2020-04-01 | GSE142541 | GEO
Project description:Plexiform neurofibromas (PNF) are benign tumors of the peripheral nervous system that represent a major source of morbidity in persons with neurofibromatosis type 1 (NF1). A significant proportion of individuals do not respond to current therapies or experience intolerable side effects. Here, we performed a systematic transcriptomic characterization of murine and human PNF at the bulk and single cell level and identified TGF-beta (TGFβ) signaling as a key upstream regulator in PNF, driving aberrant production of basement membrane (BM) proteins by both neoplastic Schwann cells and fibroblasts. Furthermore, we show that conditional overexpression of TGFβ1 in Nf1 deficient Schwann cells driven by Hoxb7-Cre promotes PNF growth and malignant transformation in vivo. Conversely, pharmacologic inhibition of the type I TGFβ receptor (TGFβRI) reduced PNF tumor burden in Nf1 mutant mice. Proteomic characterization of the extracellular matrix (ECM) revealed a reduction in BM proteins in response to TGFβRI inhibition. Collectively, these studies implicate the TGFβ pathway as a potential therapeutic target in PNF and provide insights into the role of TGFβ signaling in orchestrating ECM dynamics in the PNF microenvironment.
2025-04-03 | GSE278250 | GEO