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RNA-seq analysis of in vivo differentiated and dedifferentiated mouse Schwann cells

ABSTRACT: Schwann cells were acultely purified from intact nerves and the bridge and distal regions of transected nerves at different time-points following transection and sequenced to determine gene expression profiles of the differentiated and dedifferentiated state and its regulation by the wound microenvironment

OTHER RELATED OMICS DATASETS IN: PRJNA399857

ORGANISM(S): Mus musculus Rattus norvegicus

PROVIDER: GSE103039 | GEO | 2017/11/09

SECONDARY ACCESSION(S): PRJNA399857

REPOSITORIES: GEO

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RNA-seq analysis of in vivo differentiated and dedifferentiated mouse Schwann cells

Project description:RNA-seq analysis of in vivo differentiated and dedifferentiated mouse Schwann cells

| PRJNA399857 | ENA

c-JUN REPROGRAMS SCHWANN CELLS OF INJURED NERVES TO GENERATE A REPAIR CELL ESSENTIAL FOR REGENERATION

Project description:The striking PNS regenerative response to injury rests on the plasticity of adult Schwann cells and their ability to transit between differentiation states, a highly unusual feature in mammals. Using mice with inactivation of Schwann cell c-Jun, we show that the injury response involves c-Jun dependent natural reprograming of differentiated cells to generate a distinct Schwann cell state specialized to promote regeneration. Transected distal stumps of c-Jun mutants show 172 disregulated genes, resulting in abnormal expression of growth factors, adhesion molecules and cytoskeletal changes that lead to neuronal death, inhibition of axon growth and striking failures of functional repair after injury. These observations provide a molecular basis for understanding Schwann cell plasticity and nerve regeneration. They offer conclusive support for the notion that Schwann cells control repair in the PNS, using dedicated transcriptional controls to generate a distinct repair cell, a transition that shows similarities to transdifferentiation seen in other systems. Total RNA was purified from a 10mm segment of the distal stump and uninjured contralateral nerve from c-Jun mutants and control mice 7 days after nerve cut. For each condition (injured/uninjured) and genotype (control/ knock-out) 2 independent samples (replicates) were generated from pooled nerves of 4/6 mice resulting in a total of 8 samples: CTRL.cut.R1, CTRL.cut.R2, CTRL.uncut.R1, CTRL.uncut.R2, KO.cut.R1, KO.cut.R2, KO.uncut.R1,KO.uncut.R2.

2012-06-13 | E-GEOD-38693 | biostudies-arrayexpress

JUN Regulation of Injury-induced Enhancers in Schwann Cells

Project description:To determine gene expression differences between control transected sciatic nerves (from C57BL/6 WT mice) and mutant (Homozyous Shh 1/2/3 enhancer deletion). Our analysis revealed significant differential gene expression between the control samples and the mutants.

2022-07-27 | GSE209658 | GEO

Changes in the coding/non-coding transcriptome and DNA methylome that define the Schwann cell repair phenotype after nerve injury

Project description:Schwann cell (Büngner) repair cells play a critical role in orchestrating nerve repair after injury, but the reprogramming process that generates them is poorly understood. We present the first combined whole genome coding and non-coding RNA and CpG methylation study after nerve injury. We show that genes involved in epithelial to mesenchymal transition are enriched in repair cells and we identify long non-coding RNAs in Schwann cells. We demonstrate that the AP-1 transcription factor c-Jun regulates the expression of certain micro RNAs in repair cells, in particular miR-21 and miR-34. Surprisingly, changes in CpG methylation are limited in injury, unlike development, and restricted to specific locations, such as enhancer regions of novel Schwann cell specific genes, such as Nedd4l, and near to local enrichment of AP-1 motifs. These epigenetic changes significantly broaden our understanding of Schwann cell reprogramming in peripheral nervous system tissue repair. To identify epigenetic regulators underlying successful nerve regeneration we generated RNA-Seq, small-RNA-Seq and whole genome bisulfite sequencing libraries for uninjured nerve versus three and/or seven day post nerve transection sciatic nerves of adult C57BL/6J mice crush.

2017-08-30 | E-MTAB-5633 | biostudies-arrayexpress

Functions of HDAC1 and HDAC2 in Schwann cells during postnatal

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

Genomic characterization of well differentiated/dedifferentiated retroperitoneal liposarcoma

Project description:An integrated profiling approach was performed to define molecular alterations associated to the aggressive behavior of retroperitoneal dedifferentiated liposarcoma. In particular, matched well and dedifferentiated components as well as normal adipose tissues, obtained from the same tumor sites, were comparatively investigated to higlight differences in gene expression.

2021-03-10 | GSE159659 | GEO

Overexpression of c-Jun in mouse Schwann cells of uninjured nerves

Project description:Two mouse lines, OE/+ and OE/OE were generated expressing graded elevation (6 fold and 28 fold, respectively) of c-Jun protein selectively in Schwann cells. The effects of this on global gene expression and cellular structure in uninjured nerves was analysed during development and in the adult. Changes in gene expression and cellular arrangements were mild but detectable in c-Jun OE/+ mice, while nerves in c-Jun OE/OE mice showed obvious de-myelination and gene expression changes, including up- and down-regulation of genes previously shown to be controlled by c-Jun in Schwann cells.

2017-10-16 | E-MTAB-6138 | biostudies-arrayexpress

Genome-wide analysis of Schwann cell gene expression in LKB1-SCKO mutant mice prior to occurrence of axon degeneration

2014-08-12 | GSE60325 | GEO

Genome-wide expression analysis of murine sciatic nerve of young and old mice

Project description:The regenerative capacity of peripheral nerves declines during aging, contributing to the development of neuropathies, limiting organism function. Changes in Schwann cells prompt failures in instructing maintenance and regeneration of aging nerves; altered inflammatory environment leading to a defective Schwann cell response, as an underlying mechanism of impaired nerve regeneration during aging. Chronic inflammation was detected in intact uninjured old nerves, characterized by increased macrophage infiltration and raised levels of monocyte chemoattractant protein 1 (MCP1) and CC chemokine ligand 11 (CCL11). Schwann cells in the old nerves appeared partially dedifferentiated, accompanied by an activated repair program independent of injury. Upon sciatic nerve injury, an initial delayed immune response was followed by a persistent hyperinflammatory state accompanied by a diminished repair process. As a contributing factor to nerve aging, we showed that CCL11 interfered with Schwann cell differentiation in vitro and in vivo. Our results indicate that increased infiltration of macrophages and inflammatory signals diminish regenerative capacity of aging nerves by altering Schwann cell behavior. The study identifies CCL11 as a promising target for anti‐inflammatory therapies aiming to improve nerve regeneration in old age.

2019-09-18 | GSE137504 | GEO

Genome-wide analysis of Schwann cell gene expression in LKB1-SCKO mutant mice prior to occurrence of axon degeneration

Project description:Analysis of gene expression in LKB1(Stk11)-depleted sciatic nerves (LKB1-SCKO) vs control nerves from age-matched mice. Gene expression profiles are predominantly derived from Schwann cell glia and provide important information about the response of peripheral nerve Schwann cells to inactivation of the metabolic regulator protein LKB1(aka Stk11). Total RNA obtained from sciatic nerve segments from 6 LKB1-SCKO mutant mice compared to RNA from nerve segments from 6 control mice (floxed LKB1 mutant mice that do not express Cre recombinase).

2014-08-12 | E-GEOD-60325 | biostudies-arrayexpress

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