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Comparison of C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cells after 12 h

ABSTRACT: The aim of this study was to identify differently expressed genes between C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cells. To elucidate the unresolved mechanism behind the promoting effect of C3156-181 on PNR we cultured primary rat neonatal SCs and treated them for up to 72 h with C3 or C3156-181. We then performed gene expression microarray analysis Results from two loops of two different treatment times are summarized in this study. The samples were taken from two C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cell cultures. Microarrays were hybridized in a loop approach. Results from two loops that map to two different sampling times (loop1: after 12 hours, loop2: after 72) are compared in this study. The data in this file represents loop1. The samples were taken from untreated, C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cells.

ORGANISM(S): Rattus norvegicus

SUBMITTER: Frank Stahl

PROVIDER: E-GEOD-70747 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Comparison of C3 or C3156-181-peptide treated Isolated primary rat neonatal Sschwann Cells after 72 h

Project description:The aim of this study was to identify differently expressed genes between C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cells. To elucidate the unresolved mechanism behind the promoting effect of C3156-181 on PNR we cultured primary rat neonatal SCs and treated them for up to 72 h with C3 or C3156-181. We then performed gene expression microarray analysis Results from two loops of two different treatment times are summarized in this study. The samples were taken from two C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cell cultures. Microarrays were hybriszed in a loop approach. Results from two loops that map to two different sampling times (loop1: after 12 hours, loop2: after 72) are compared in this study. The data in this file represents loop2. The samples were taken from The samples were taken from untreated, C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cells.

2015-07-11 | E-GEOD-70748 | biostudies-arrayexpress

Comparison of C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cells after 12 h

2015-07-11 | GSE70747 | GEO

Comparison of C3 or C3156-181-peptide treated Isolated primary rat neonatal Sschwann Cells after 72 h

2015-07-11 | GSE70748 | GEO

Project description:Comparison of C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cells

| PRJNA289482 | ENA

Rattus norvegicus

Project description:Comparison of C3 or C3156-181-peptide treated Isolated primary rat neonatal Schwann Cells after 12 h

| PRJNA289484 | ENA

Rattus norvegicus

Project description:Comparison of C3 or C3156-181-peptide treated Isolated primary rat neonatal Sschwann Cells after 72 h

| PRJNA289485 | ENA

Algesic MBP peptide induce pain-specific signaling in rodent Schwann Cells

Project description:We demonstrated the pain-specific response to the algesic peptide fragment MBP84-104 of myelin basic protein that induces pain if injected into sciatic nerve of rats and mice. We used the wild-type peptide MBP 84-104, H89G mutant peptide (MBP84-104-H89G), scramble peptide (MBP84-104-SCR) and phosphomimetic peptide MBP84-104-mimTT to stimulate the primary rat Schwann cell cultures. After 24h we isolated total RNA and conducted genome wide RNA-seq. In addition, we performed RNA-seq using Schwann cells constitutively expressing an MBP84-104-mCherry construct. The gene expression data was analyzed using Ingenuity Pathway Analysis software. We conclude that the Schwann cells expressing MBP84-104 constructs stimulate pain-specific signaling pathways thus representing a relevant model to study neuropathic pain.

2018-08-13 | GSE107020 | GEO

Transcription profiling of rat neonatal ventricular cardiac mycocytes exposed to endothelin-1 and C3 toxin

Project description:Effects of C3 toxin on RNA profiles in neonatal rat ventricular cardiac myocytes exposed to endothelin-1 (1 h)

2010-05-25 | E-MEXP-1977 | biostudies-arrayexpress

Cell transplantation strategies for acquired and inherited disorders of peripheral myelin

Project description:Objective: To investigate transplantation of rat Schwann cells or human iPSC-derived neural crest cells and derivatives into models of acquired and inherited peripheral myelin damage. Methods: Primary cultured rat Schwann cells labeled with a fluorescent protein for monitoring at various times after transplantation. Human induced pluripotent stem cells (iPSCs) were differentiated into neural crest stem cells (NCSC), and subsequently toward a Schwann cell lineage via two different protocols. Protocol 1 = treated with MesenPRO with Heregulin. Protocol 2 = coculture with iPSC-derived Motor Neurons. Cell types were characterized using flow cytometry, immunocytochemistry and transcriptomics. Rat Schwann cells and human iPSC-derivatives were transplanted into (i) nude rats pretreated with lysolecithin to induce demyelination or (ii) a transgenic rat model of dysmyelination due to PMP22 overexpression. Results: Rat Schwann cells transplanted into sciatic nerves with either toxic demyelination or genetic dysmyelination engrafted successfully, and migrated longitudinally for relatively long distances, with more limited axial migration. Transplanted Schwann cells engaged existing axons and displaced dysfunctional Schwann cells to form normal appearing myelin. Human iPSC-derived neural crest stem cells and their derivatives shared similar engraftment and migration characteristics to rat Schwann cells after transplantation, but did not further differentiate into Schwann cells or form myelin. Interpretation: These results indicate that cultured Schwann cells surgically delivered to peripheral nerve can engraft and form myelin in either acquired or inherited myelin injury, as proof of concept for pursuing cell therapy for diseases of peripheral nerve. However, lack of reliable technology for generating human iPSC-derived Schwann cells for transplantation therapy remains a barrier in the field.

2018-01-26 | GSE109686 | GEO

BioID study of the PHB2 interactome in Schwann cells and how it changes depending on neuronal signals

Project description:Schwann cells are critical for the proper development and function of the peripheral nervous system, where they form a collaborative relationship with axons. Past studies highlighted that a pair of proteins called the prohibitins play major roles in Schwann cell biology. Prohibitins are ubiquitously expressed and versatile proteins. We have previously shown that while prohibitins play a crucial role in Schwann cell mitochondria for long-term myelin maintenance and axon health, they may also be present at the Schwann cell-axon interface during development. The current data set uses BioID to identify a pool of candidate PHB2 interactors in Schwann cells and explores how the PHB2 interactome changes depending on neuronal signals. We expressed a PHB2-turboID fusion construct in primary rat Schwann cells; turboID is a 35 kDa engineered biotin ligase that rapidly biotinylates proximal proteins. Thus, proteins interacting with PHB2-turboID within an approximately 10 nm radius are tagged with biotin. As a control, primary rat Schwann cells were transfected with an unfused turboID construct (Con-turboID). Schwann cells expressing Con-turboID or PHB2-turboID were plated alone or onto primary rat DRG neurons, in the presence or absence of biotin. After 2 hours, proteins were harvested from the cultures and biotinylated proteins were purified using streptavidin-affinity purification (AP). We then used liquid chromatography-mass spectrometry (LC-MS) to identify the PHB2-turboID interactors (the biotinylated proteins) in our purified pool. The PHB2 interactors identified here, especially those which increase or decrease interaction with PHB2-turboID in the presence of neurons, may play a role in prohibitin-associated Schwann cell-axon communication.

2024-09-02 | PXD054241 | Pride

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