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The Refilin/Filamin complex regulates filipodia dynamics in oligodendrocyte progenitor cells.

ABSTRACT: Actin assembly and dynamics control the shape, motility and functions of diverse cell types. Programme for controlling theses dynamics is hard-coded into actin binding proteins and regulatory proteins. Refilins (RefilinA and RefilinB) are short lived regulatory proteins that interact with the actin-binding protein Filamin to convert it from an actin branching protein into one that bundles. We here show that different mechanisms converge to increase Refilin level in brain NG2+ precursor cells (polydendrocytes) committed to differentiate into the oligodendrocyte lineage. RefilinA is up-regulated through transcriptional activation during commitment into oligodendrocyte progenitor cells (OPC). RefilinB expression relies on PDGF signalling and is further stabilized by a unique auto-inhibitory domain masking the adjacent conserved PEST degradation signal. In NG2+ precursor cells and OPC, the RefilinB/Filamin complex localizes on filipodia protrusions and filipodial processes. Stable ectopic expression of Refilins in cells stimulates membrane remodelling dynamics linked with filipodia growth. These studies extend the function of the Refilin/FLNA complex to cell membrane remodelling linked with reorganization of underlying actin cytoskeleton. We performed whole transcriptomic analysis on the three cell population derived from OPC cells. Three different cultures were done and for each experiment we compared each cell population (NG2+, NG2+/A2B5 and O4) to the other 2 cell populations.

ORGANISM(S): Rattus norvegicus

SUBMITTER: jacques Baudier

PROVIDER: E-GEOD-37600 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The Refilin/Filamin complex regulates filipodia dynamics in oligodendrocyte progenitor cells.

Project description:Actin assembly and dynamics control the shape, motility and functions of diverse cell types. Programme for controlling theses dynamics is hard-coded into actin binding proteins and regulatory proteins. Refilins (RefilinA and RefilinB) are short lived regulatory proteins that interact with the actin-binding protein Filamin to convert it from an actin branching protein into one that bundles. We here show that different mechanisms converge to increase Refilin level in brain NG2+ precursor cells (polydendrocytes) committed to differentiate into the oligodendrocyte lineage. RefilinA is up-regulated through transcriptional activation during commitment into oligodendrocyte progenitor cells (OPC). RefilinB expression relies on PDGF signalling and is further stabilized by a unique auto-inhibitory domain masking the adjacent conserved PEST degradation signal. In NG2+ precursor cells and OPC, the RefilinB/Filamin complex localizes on filipodia protrusions and filipodial processes. Stable ectopic expression of Refilins in cells stimulates membrane remodelling dynamics linked with filipodia growth. These studies extend the function of the Refilin/FLNA complex to cell membrane remodelling linked with reorganization of underlying actin cytoskeleton.

2013-05-01 | GSE37600 | GEO

gene expression profiling in CD69 positive blood cells selected from Healthy blood Donors and HTLV-1-infected patients

Project description:The goal of the study was to identify difference in gene expression between activated /CD69+ blood cells selected from HTLV-1-infected patient displaying HAM-TSP disease (HTLV-1-associated myelopathy/tropical spastic paraparesis), compared to healthy blood donor /HD (biological sample providers: Dr. Antoine Gessain, Pasteur Institute Paris and Etablissement FranM-CM-'ais du Sang) We performed microarray gene expression profiling of Immune cells selected on the marker of early activation, CD69, by the use of MACS beads (Miltenyi Biotec), from 10.106 blood cells of two healthy blood donors and two HAM/TSP patients

2012-03-14 | E-GEOD-33859 | biostudies-arrayexpress

Microarray gene expression profiling in central neurocytomas

Project description:Microarray gene expression profiling of central neurocytomas (CNs). Comparison between neurocytoma, pineocytoma (PC) and pineoblastoma (PB) relative to normal brain. Gene expression analysis was performed on tumor samples. Tumor tissues of 5 CNs, 2 PCs (low-grade pineal parenchymal tumors (PPTs)) and 2 PBs (high-grade PPTs) were obtained from the NeurobiotecBank (Groupement Hospitalier Est, Bron, France) or from the AP-HM Tissue Bank (Assistance Publique-HM-CM-4pitaux de Marseille, France). At surgery, the tumor tissue was divided into 2 fragments, one of which was frozen and stored in liquid nitrogen for RNA extraction, whereas the other was fixed for histopathologic analysis.

2013-02-19 | E-GEOD-35499 | biostudies-arrayexpress

Transcriptomic dysregulation in aggressive and malignant prolactin tumours

Project description:Pituitary tumours are generally benign. However, many are invasive and some of these are aggressive with high proliferation and recurrence rates. Only metastatic tumours are considered malignant and are rare (0.2%). To identify molecular events associated with the aggressive and malignant phenotypes, we combined a comparative genomic hybridization and transcriptomic analysis of 13 prolactin (PRL) tumours classified as non-invasive (NI; n=5), invasive (I; n=2) or aggressive-invasive (AI; n=6). Each tumour showed copy number alterations which appeared to be varied and discrete in the NI and I tumour groups, and more numerous and extensive in the AI tumour group. Allelic loss within the p arm region of chromosome 11 was detected in five of the AI tumours. This region contains the cytobands 11p15.2, 11p15.1, 11p14.3, 11p14.2, 11p14.1, 11p13, 11p12 and 11p11.2. Furthermore, an allelic loss in the 11q arm was also observed in three of these five tumours, which were considered malignant based on the presence of metastases. The comparison of genomic and transcriptomic data showed that allelic loss impacted upon the expression of genes located in the imbalanced region. An original data filtering strategy allowed us to highlight five genes (DGKZ, CD44, TSG101, GTF2H1 and HTATIP2), within the missing 11p region, potentially responsible for triggering the aggressive and malignant phenotypes of PRL tumours. Our novel combined genomic and transcriptomic analysis underlines the importance of chromosome 11 allelic loss in aggressive and malignant PRL tumours and led us to propose a new strategy to find markers of progression in rare tumours. Transcriptomic analysis of Codelink Human Whole Genome Bioarray was performed for 13 prolactin tumors: 6 aggressive-invasive, 2 invasive, and 5 non-invasive.

2011-03-16 | E-GEOD-22812 | biostudies-arrayexpress

CCN5, a novel transcriptional repressor

Project description:CCN5 is a member of the CCN (Connective Tissue Growth Factor/Cysteine-rich 61/Nephroblastoma overexpressed) family and was identified as an estrogen-inducible gene in estrogen receptor-positive cell lines. However, the role of CCN5 in breast carcinogenesis remains unclear. We report here that CCN5 protein is localized mostly in the cytoplasm, and in part in the nucleus, of human tumor breast tissue. Using a heterologous transcription assay, we demonstrate that CCN5 can act as a transcriptional repressor, presumably through association with histone deacetylase HDAC1. Microarray gene expression analysis showed that CCN5 represses expression of genes associated with epithelial-mesenchymal transition (EMT) as well as expression of key components of the TGF-beta signaling pathway, prominent among them TGF-betaRII receptor. We show that CCN5 is recruited to the TGF-betaRII promoter, thereby providing a mechanism by which CCN5 restricts transcription of the TGF-betaRII gene. Consistent with this finding, we found that CCN5 functions to suppress TGF-beta-induced transcriptional responses and invasion that is concomitant with EMT. Thus, our data uncovered CCN5 as a novel transcriptional repressor that plays an important role in regulating tumor progression functioning, at least in part, by inhibiting the expression of genes involved in the TGF-beta signaling cascade that is known to promote EMT. We performed microarray gene expression profiling of one MCF-7-sh-CCN5 sample and one MCF-7-sh-scrambled sample (control sample).

2011-11-30 | E-GEOD-25431 | biostudies-arrayexpress

Molecular Characterization of Laser Microdissected Circumventricular Organs and Third Ventricle Ependyma in the Adult Rat by Microarray Analysis.

Project description:We used LCM and microarrays to analyze the transcriptomes of three CVOs, the SCO, the subfornical organ (SFO), and the PG, and the third ventricle ependyma in the adult rat in order to better characterize these organs at the molecular level. Gene expression was performed on laser microdissection of rat Pineal Gland (n=2), Subcommisural Organ (pool of 2), Subfornical Organ (pool of 2) and Third Ventricle Ependyma (pool of 2). Pool of rat total normal brains was used as reference.

2012-05-23 | E-GEOD-35089 | biostudies-arrayexpress

Genomic alterations of chromosome 11 induce transcriptome dysregulation in aggressive and malignant prolactin tumours

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2011-09-15 | E-GEOD-32191 | biostudies-arrayexpress

Identification of the most immunoreactive antigens of Candida auris to sera from infected mice

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2024-06-23 | PXD049077 | Pride

Gene Expression Analysis of Nestin-creERT2, or NG2-creERTM driven P53f/f; Nf1f/+; Ptenf/+ mouse GBM

Project description:We have developed spontaneous genetically engineered GBM mouse models from two distinct cells of origin: subventricular zone neural stem cells (SVZ; Nestin-creERT2) and oligodendrocyte lineage progenitor cells (OPC; NG2-creERTM). These tumors are biologically separable and are reflective of their lineage of origin.

2020-03-31 | GSE127273 | GEO

Rapid differentiation of hiPSCs into functional oligodendrocytes using an OLIG2 synthetic modified messenger RNARapid differentiation of hiPSCs into functional oligodendrocytes using an OLIG2 synthetic modified messenger RNA

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