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Nell-1 primary response gene

ABSTRACT: We hypothesized that Nell-1, as a growth factor, is supposed to stimulate some molecular mediators, which transmit signals to downstream and finally affect chondrogenic differentiation. The molecular mediators which respond to Nell-1 in short time are our research objects, we called them primary response genes referred to pervious report . To find out Nell-1 primary response gene candidates, we first used microarray assays to analyze the differences of gene expression profile between rhNell-1 protein (100 ng/ml) and control (PBS) treatment.

ORGANISM(S): Mus musculus

PROVIDER: GSE23570 | GEO | 2010/09/01

SECONDARY ACCESSION(S): PRJNA130927

REPOSITORIES: GEO

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Nell-1 primary response gene

Project description:We hypothesized that Nell-1, as a growth factor, is supposed to stimulate some molecular mediators, which transmit signals to downstream and finally affect chondrogenic differentiation. The molecular mediators which respond to Nell-1 in short time are our research objects, we called them primary response genes referred to pervious report . To find out Nell-1 primary response gene candidates, we first used microarray assays to analyze the differences of gene expression profile between rhNell-1 protein (100 ng/ml) and control (PBS) treatment. For screening real primary response genes, which is not regulated by new synthesis protein, ATDC5 cells were subjected to serum starvation, followed by protein synthesis inhibitor CHX (10 μg/ml) treatment for 30 min and then treated with PBS (control) or rhNell-1 protein (100 ng/ml) for another 30 min. Cell total RNA samples were sent to the UCLA DNA Microarray Centre (Los Angeles, CA) where target preparation and hybridization to the Affymetrix Murine 430 2.0 GeneChip was carried out following the standard protocol (http://www.affymetrix.com). This GeneChip contains over 39,000 full-length mouse genes and EST clusters from the UniGene database. The data obtained from the hybridization was preprocessed using Affymetrix GeneChip Command Console Software (AGCC) and Expression Console Software to generate probe set intensity data (Affymetrix, Santa Clara, CA). Expression values were further filtered by retaining only those probe sets with a fold change of at least 1.5 in rhNell-1 protein treatment samples compared with controls.

2010-09-01 | E-GEOD-23570 | biostudies-arrayexpress

Mus musculus

Project description:Nell-1 primary response gene

| PRJNA130927 | ENA

CNTNAP4 signaling regulates osteosarcoma disease progression

Project description:Improved treatment strategies for sarcoma rely on clarification of the molecular mediators of disease progression. Recently, we identified the secreted glycoprotein NELL1 modulates osteosarcoma (OS) disease progression in part via altering the sarcomatous extracellular matrix and cell-ECM interactions. Of known NELL1 interactor proteins, Contactin-associated protein-like 4 (Cntnap4) encodes a member of the neurexin superfamily of transmembrane molecules best known for its presynaptic functions in the central nervous system. Here, CRISPR/Cas9 gene deletion of CNTNAP4 reduced OS tumor growth, sarcoma-associated angiogenesis, and pulmonary metastases. CNTNAP4 knockout (KO) in OS tumor cells largely phenocopied the effects of NELL1 KO, including reductions in sarcoma cell attachment, migration, and invasion. Moreover, CNTNAP4 KO cells were unresponsive to the effects of NELL1 treatment. Transcriptomic analysis combined with protein phosphoarrray demonstrated notable reductions in MAPK signaling with CNTNAP4 deletion, the ERK agonist isoproterenol restored OS cell functions among CNTNAP4 KO tumor cells. Finally, human primary cells and tissues in combination with publicly available sequencing data confirmed the significance of CNTNAP4 signaling in human sarcomas. In summary, our findings demonstrate the biological importance of NELL-1/CNTNAP4 signaling in disease progression of human sarcomas and suggest that targeting NELL-1/CNTNAP4 signaling represents a strategy with therapeutic benefit in sarcoma patients.

2023-01-11 | GSE210373 | GEO

Expression data from differently treated mouse cardiomyocytes

Project description:We wanted to analyze the global gene expression to unravel molecular mechanisms underlying the combined action of DOX and IFNγ in mouse cardiomyocytes. We treated the cardiomyocytes respectively with PBS, DOX and DOX plus IFN-γ, and the differentially expressed genes and the gene expression patterns were supposed to be analyzed.

2020-11-17 | GSE107113 | GEO

Immunoresolving lipid mediators support effective skeletal muscle repair

Project description:Specialized pro-resolving mediators (SPMs) function to limit inflammation and actively stimulate

2020-03-12 | GSE146785 | GEO

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and NELL-1(+/6R) Mouse Hippocampus Transcriptomes

Project description:The goal of this study is to profile and compare the hippocampus transcriptomes of wild type (WT) and NELL-1(+/6R) mice to gain insight on their neurological function.

2023-12-20 | GSE180856 | GEO

NELL-1 regulates the matrisome to alter osteosarcoma disease progression

Project description:Sarcomas produce abnormal extracellular matrix (ECM) which in turn provides instructive cues for cell growth and invasion. Neural EGF Like-Like molecule 1 (NELL-1) is a secreted glycoprotein characterized by its non-neoplastic osteoinductive effects, yet highly expressed in skeletal sarcomas. Here, NELL1 gene deletion markedly reduced invasive behavior across human osteosarcoma (OS) cell lines. This resulted in reduced OS disease progression, inhibited metastatic potential and improved survival in a xenograft model. These observations were recapitulated with Nell1 conditional knockout in mouse models of p53/Rb driven sarcomagenesis, including reduced tumor frequency, and extended tumor free survival. Transcriptomic and phospho-proteomic analysis demonstrated NELL1 loss skews the expression of matricellular proteins associated with reduced FAK signaling. Culture on OS enriched matricellular proteins reversed phenotypic and signaling changes among NELL1 knockout sarcoma cells. These findings in mouse and human models suggest that NELL-1 expression alters the sarcoma matrix, thereby modulating cellular invasive potential and prognosis. Disruption of NELL-1 signaling may represent a novel therapeutic approach to short circuit sarcoma disease progression.

2022-08-10 | GSE182703 | GEO

Matrix reverses immortalization-mediated stem cell fate determination

Project description:Primary cell culture in vitro suffers from cellular senescence. We hypothesized that expansion on decellularized extracellular matrix (dECM) deposited by simian virus 40 large T antigen (SV40 LT) transduced autologous infrapatellar fat pad stem cells (IPFSCs) could rejuvenate high-passage IPFSCs in both proliferation and chondrogenic differentiation. In the study, we found that SV40 LT transduced IPFSCs exhibited increased proliferation and adipogenic potential but decreased chondrogenic potential. Expansion on dECMs deposited by passage 5 IPFSCs yielded IPFSCs with dramatically increased proliferation and chondrogenic differentiation capacity; however, this enhanced capacity diminished if IPFSCs were grown on dECM deposited by passage 15 IPFSCs. Interestingly, expansion on dECM deposited by SV40 LT transduced IPFSCs yielded IPFSCs with enhanced proliferation and chondrogenic capacity but decreased adipogenic potential, particularly for the dECM group derived from SV40 LT transduced passage 15 cells. Our immunofluorescence staining and proteomics data identify matrix components such as basement membrane proteins top candidates for matrix mediated IPFSC rejuvenation. Both cell proliferation and differentiation were endorsed by transcripts measured by RNASeq during the process. This study provides a promising model for in-depth investigation of matrix protein influence on surrounding stem cell differentiation.

2022-02-16 | PXD021069 | Pride

Expression data in CD4 T cells from lungs of PBS or house dust mite treated mice

Project description:CD4 T cells are essential mediators of the asthmatic process. We used the clinically relevant allergen house dust mites to induce signs of allergy in mice and performed gene expression arrays specifically on CD4 T cells infiltrating the lung Reference: IL-21-producing CD4+ T cells promote type 2 immunity to house dust mites Primary CD4+ T cells were isolated from mice sensitised and challenged to either house dust mites or PBS. Purification of CD4 T cells was performed by flow cytometry. RNA was isolated, converted to cDNA and then hybridised on Affymetrix GeneChip Mouse Gene 2.0 ST Arrays

2015-08-13 | E-GEOD-72005 | biostudies-arrayexpress

1H NMR metabolite monitoring during the differentiation of human induced pluripotent stem cells provides new insights into the molecular events that regulate embryonic chondrogenesis

Project description:The integration of cell metabolism with signalling pathways, transcription factor networks and epigenetic mediators is critical in coordinating molecular and cellular events during embryogenesis. Induced pluripotent stem cells (IPSCs) are an established model for embryogenesis, germ layer specification and cell lineage differentiation, advancing the study of human embryonic development and the translation of innovations in drug discovery, disease modelling and cell-based therapies. The metabolic regulation of IPSC pluripotency is mediated by balancing glycolysis and oxidative phosphorylation, but there is a paucity of data regarding the influence of individual metabolite changes during cell lineage differentiation. We used <sup>1</sup>H NMR metabolite fingerprinting and footprinting to monitor metabolite levels as IPSCs are directed in a three-stage protocol through primitive streak/mesendoderm, mesoderm and chondrogenic populations. Metabolite changes were associated with central metabolism, with aerobic glycolysis predominant in IPSC, elevated oxidative phosphorylation during differentiation and fatty acid oxidation and ketone body use in chondrogenic cells. Metabolites were also implicated in the epigenetic regulation of pluripotency, cell signalling and biosynthetic pathways. Our results show that <sup>1</sup>H NMR metabolomics is an effective tool for monitoring metabolite changes during the differentiation of pluripotent cells with implications on optimising media and environmental parameters for the study of embryogenesis and translational applications.

2023-05-24 | MTBLS4854 | MetaboLights

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