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Gene-expression analysis of human embryonic stem cell (HESC-)- derived rosette-forming neural progenitor cells (NPCs) in the presence of lysophosphatidic acid (LPA)

ABSTRACT: Gene-expression analysis of human embryonic stem cell (HESC-)- derived rosette-forming neural progenitor cells (NPCs) in the presence of lysophosphatidic acid (LPA)

PROVIDER: PRJNA437487 | ENA |

REPOSITORIES: ENA

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Gene-expression analysis of human embryonic stem cell (HESC-)- derived rosette-forming neural progenitor cells (NPCs) in the presence of lysophosphatidic acid (LPA)

Project description:As part of our study on the effect of LPA on HESC-derived NPCs, we have employed whole genome microarray analysis to identify genes which were up- and downregulated in the presence of LPA compared to non-LPA-treated control-NPCs and which might be involved in the expansion of the apical domain of NPCs and large rosette formation that we observe after LPA-treatment.

2018-03-14 | GSE111597 | GEO

Influence of lysophosphatidic acid (LPA) and LPA together with interferon tau (IFNt) on transcriptional profiling of bovine endometrial cells.

2014-01-10 | GSE53457 | GEO

Human gingival fibroblasts: control vs. lysophosphatidic acid (LPA 18:1)-treated

Project description:Transcriptional profiling of pass 2 primary human gingival fibroblasts (GF) comparing control untreated GF with GF treated with LPA 18:1 for 2h or 8h. The goal of this study was to determine the effects of LPA 18:1 on global GF gene expression. Three-condition experiment, GF vs. LPA-treated (2h, 8h) GF cells. Biological replicates: 3 control replicates, 3 LPA-treated replicates.

2014-05-12 | E-GEOD-57496 | biostudies-arrayexpress

Human gingival fibroblasts: control vs. lysophosphatidic acid (LPA 18:1)-treated

2014-05-12 | GSE57496 | GEO

Influence of lysophosphatidic acid (LPA) and LPA together with interferon tau (IFNt) on transcriptional profiling of bovine endometrial cells.

Project description:The endometrium plays a crucial role in the reproductive organs in the aspect of embryo-maternal communication and pregnancy. This study investigated transcriptome profiles of endometrial cells stimulated with PBS, LPA and LPA in combination with IFNt. LPA, one of the signaling molecule, is locally produced and released from the bovine endometrium during estrous cycle and early pregnancy. The highest concentration of LPA and expression of its active receptor (LPAR1) were detected in bovine endometrium at the time of maternal recognition of pregnancy, when the conceptus announces its presence by increased IFNt production. Using transcriptomic approach we compared the influence of LPA and LPA together with IFNt on the gene expression profiles in bovine endometrial cells. A total of nine normally cycling Holstein/Polish Black and White (75/25% respectively) cows were used in this study. Global transcriptional profiling was performed using co-cultured stromal and epithelial cells (ratio - 3:1) isolated from bovine endometrium. Three experimental conditions (control (PBS), LPA and LPA plus IFNt) with three replicates per condition were prepared. Total RNAs were extracted from 9 pooled samples (n=3 for each sample) amplified and hybridized onto Affymetrix microarrays.

2014-01-10 | E-GEOD-53457 | biostudies-arrayexpress

Expression of autotaxin and lysophosphatidic acid receptors increases mammary tumorigenesis, invasion, and metastases

Project description:Lysophosphatidic acid (LPA) acts through high-affinity G protein-coupled receptors to mediate a plethora of physiological and pathological activities associated with tumorigenesis. LPA receptors and autotaxin (ATX/LysoPLD), the primary enzyme producing LPA, are aberrantly expressed in multiple cancer lineages. However, the role of ATX and LPA receptors in the initiation and progression of breast cancer has not been evaluated. We demonstrate that expression of ATX or each edg family LPA receptor in mammary epithelium of transgenic mice is sufficient to induce a high frequency of late-onset, estrogen receptor (ER)-positive, invasive, and metastatic mammary cancer. Thus, ATX and LPA receptors can contribute to the initiation and progression of breast cancer.

2009-06-11 | GSE15263 | GEO

Lysophosphatidic acid (LPA)-dependent propagation of neuroinflammation in an optimized model of post-hemorrhagic hydrocephalus.

Project description:Post-hemorrhagic hydrocephalus (PHH) is a neurological disease that primarily affects premature infants and involves infiltration of blood into the brain’s ventricles followed by excessive accumulation of cerebrospinal fluid (CSF) leading to ventricular enlargement and increased intracranial pressure. However, the precise mechanisms driving PHH development and persistence remain incompletely known and lack medical and disease modifying treatments. Here we use a mouse model of PHH to identify transcriptomic, proteomic and cellular changes involving neurovascular and neuroimmunological microglial alterations as features of PHH, overlapping with those reported in human disease. Improvements on a lysophosphatidic acid (LPA)-initiated PHH mouse model were developed and combined with unbiased proteomic and single-nucleus transcriptomics that identified microglial molecular pathways promoting PHH. Pharmacological disruption of microglia in vivo significantly reduced PHH-associated ventriculomegaly. These data identify microglia and neurovascular molecular elements in the development of PHH, implicating them as potentially tractable therapeutic targets towards developing new treatments for PHH.

2025-05-22 | GSE272062 | GEO

Identification of LPA-LPAR-GNA12 driven Gene signatures and Key Pathways in Ovarian Cancer

Project description:Lysophosphatidic acid (LPA) and LPA-receptor (LPAR)-activated G-protein alpha subunits encoded by GNAi2, GNA12, and GNA13 play a crucial role in ovarian cancer progression. While the general signaling mechanism regulated by LPA-LPAR-signaling had previously been characterized, the global transcriptomic network regulated by individual G protein alpha-subunits in ovarian cancer pathophysiology remains largely unknown. To define the specific oncogenic networks regulated by LPA-stimulated GNAi2, GNA12, and GNA13 in ovarian cancer, transcriptomic analyses were carried out using SKOV3 cells in which the expression of GNAi2, GNA12, or GNA134 was silenced in an Agilent SurePrint G3 Human Comparative Genomic Hybridization 8x60 microarray platform.

2021-08-25 | GSE173214 | GEO

Transcriptomic analysis of human breast and prostate cancer cell lines on lysophosphatidic acid (LPA) stimulation

Project description:LPA is a natural bioactive lipid with growth factor-like functions due to activation of series of six G protein-coupled receptors (LPA1-6). In this study we determine the LPA induced early-gene expression profile in three unrelated human cancer cell lines (MDA-MB-231, MCF7, PC3) with an objective to identify potential biomarker/s specifically upregulated through the activation of LPA receptor type 1 (LPA1)

2014-05-16 | GSE56265 | GEO

Tumor-derived Lysophosphatidic Acid Blunts Protective Type-I Interferon Responses in Ovarian Cancer

Project description:Lysophosphatidic acid (LPA) is a bioactive lipid enriched in highly immunosuppressive neoplasms like ovarian cancer (OvCa). While LPA is known to enhance the tumorigenic capacity of malignant cells, the immunomodulatory role of this phospholipid in cancer remains largely unexplored. Here, we report that LPA operates as a negative regulator of type-I interferon (IFN) responses in OvCa. Ablation of the LPAgenerating enzyme autotaxin in OvCa cells reprogrammed the tumor immune microenvironment, extended host survival, and improved the effects of therapies that elicit protective responses driven by type-I IFN. Mechanistically, LPA sensing by dendritic cells triggered PGE2 synthesis that suppressed type-I IFN signaling via autocrine EP4 engagement. Moreover, we identified an LPA-controlled, immune-derived gene signature associated with weak responses to combined PARP inhibition and PD-1 blockade in OvCa patients. Controlling LPA production or sensing in tumors may therefore be useful to improve cancer immunotherapies that rely on robust induction of type-I IFN.

2022-08-02 | GSE182062 | GEO

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