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.
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 hybridized in a loop approach.
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 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.
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.
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.
Project description:Our aim is to explore the effect of Hydroxy-carboxylic Acid Receptor 1 on cardiomyocytes. Neonatal rat cardiomyocytes (NRCMs) were isolated and cultured. Subsequently, NRCMs were treated with the agonist of Hydroxy-carboxylic Acid Receptor 1 (HCAR1), 3Cl-HBA at 40 μM for 48 h(HBA1,HBA2 and HBA3) or DMSO as control(C1,C3 and C3). RNA was extracted using the KAPA RiboErase RNA-Seq kit (Roche, Basel, Switzerland), and was analysed using the Agilent Bioanalyzer 2100 system (Agilent Technologies, CA, USA) for quality control. The libraries were sequenced on an Illumina HiSeq X Ten platform. DESeq2 was used to analyse RNA-seq data. Neonatal rat cardiomyocytes (NRCMs) were isolated and cultured. Subsequently, NRCMs were treated with the agonist of Hydroxy-carboxylic Acid Receptor 1 (HCAR1), 3Cl-HBA (40 μM for 48 h) or DMSO as control. RNA was extracted using the KAPA RiboErase RNA-Seq kit (Roche, Basel, Switzerland), and was analysed using the Agilent Bioanalyzer 2100 system (Agilent Technologies, CA, USA) for quality control. The libraries were sequenced on an Illumina HiSeq X Ten platform.
Project description:miR-222 overexpression leads to promotion of proliferation and hypertrophy and inhibition of apoptosis in in primary neonatal rat ventricular cardiomyocytes (NRVMs). Isolated primary neonatal rat ventricular cardiomyocytes were plated in 6 cm BD Primaria tissue culture dishes. Transfection of microRNA precursors or scramble control (0.4 μM) was carried out using Lipofectamine RNAiMAX (Invitrogen) as recommended by the manufacturer. Forty-eight hours after transfection, RNAs from cultured cells and tissues were isolated with Tryzol (Invitrogen) following the manufactures’ manuals. Total RNA was harvested and submitted to the Dana-Farber Cancer Institute Molecular Diagnostics Laboratory for assay. These results revealed miR-222 regulated gene expression in primary neonatal rat ventricular cardiomyocytes.