Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA246749 | ENA |
REPOSITORIES: ENA
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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
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.
2014-05-12 | GSE57496 | GEO
Project description:We screened highly expressed G-protein coupled receptors (GPCRs) in normal human epidermal keratinocytes (NHEKs). We then tested the effect of ligands of selected GPCRs for their potency to induce the expression of FLG, a crucial skin barrier marker gene, in NHEKs. We used CP-609,550, a JAK inhibitor, as a positive control. As a result, we identified Oleoyl-L-α-lysophosphatidic acid (LPA) as a strong FLG inducer in NHEKs. In addition, we found that LPA induced NHEKs morphological changes characteristics of differentiated keratinocytes. Notably, although CP-609,550 also induced FLG expression in NHEKs, it didn't affect NHEKs cell morphology. We further conducted comprehensive and comparative microarray analysis of gene expression induced by LPA and CP-609,550 in NHEKs. We found that LPA treatment not only induced FLG expression but also expression of several genes related to keratinocytes differentiation, epidermis development and cornified envelope. This was not observed in the CP-609,550-treated cells.
2018-11-01 | GSE122023 | GEO
Project description:We report the differential gene expression patterns of TILs from two patients after treating the cells with lysophosphatidic acid (LPA) for 2 or 3 hours. Among the common LPA-regulated genes are transcription factors and other immediate early genes as well as T-cell regulatory cell-surface molecules
2023-01-15 | GSE143697 | GEO
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
Project description:Autotaxin (ATX, Enpp2) is a secreted lysophospholipase D catalyzing the production of lysophosphatidic acid (LPA), a pleiotropic growth factor-like phospholipid. Upregulated ATX expression has been detected in various chronic inflammatory disorders and different types of cancer; among them increased ATX mRNA or immunohistochemical staining has been suggested in Hepatocellular carcinoma (HCC) patients. Conditional deletion of ATX/Enpp2 specifically from hepatocytes, in AlbEnpp2-/- mice, attenuated the DEN/CCl4-mediated HCC development in mice. To obtain mechanistic insights into the mode of action of the ATX/LPA axis in HCC development, we performed whole liver, genome wide expression profiling of DEN/CCl4-induced HCC upon the genetic deletion of Autotaxin (ATX) in AlbEnpp2-/- mice in comparison with DEN/CCl4-treated and untreated wt littermate mice.
2016-11-30 | E-MTAB-4648 | biostudies-arrayexpress
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
Project description:Myosin Vb (Myo5b) is an essential trafficking protein for membrane recycling in gastrointestinal (GI) epithelial cells and its inactivating mutation causes the congenital diarrheal disease, microvillus inclusion disease (MVID). We previously reported that Myo5b deficiency in mice causes mislocalization of SGLT1 and NHE3, but retained apical function of CFTR, resulting in malabsorption and secretory diarrhea. Activation of lysophosphatidic acid (LPA) receptors can improve diarrhea, but the effects of LPA on MVID symptoms is unclear. We therefore tested whether LPA treatment can ameliorate the epithelial deficits in Myo5b knockout (KO) mice. Methods: Adult tamoxifen-induced, intestine-specific, Myo5b KO (VillinCreERT2;Myo5bflox/flox) and littermate control mice were treated with LPA, an LPAR2 agonist (GRI977143), or vehicle for 4 days after a single tamoxifen injection. Apical SGLT1 and CFTR activities were measured in Üssing chambers. The localization of membrane transporters was evaluated by immunostaining in mouse tissues and enteroids. RNA sequencing and enrichment analysis were performed with isolated jejunal epithelial cells. Results: Daily treatment with LPA decreased the frequency of multivesicular bodies and the expression of cathepsins, but did not affect the formation of microvillus inclusions in Myo5b KO mice. LPA partially restored the brush border height and the localization of SGLT1 and NHE3 in Myo5b KO small intestine and enteroids. SGLT1-dependent short-circuit current (Isc) was increased and abnormal CFTR activities were suppressed in LPA-treated jejunum compared to that of vehicle-treated Myo5b KO mice. Conclusions: Cell autonomous LPA signaling may modulate a Myo5b-independent trafficking mechanism and the brush border maturation, demonstrating a therapeutic potential for LPA in the treatment of MVID.
2019-10-24 | GSE139302 | GEO
Project description:We used a fractionation scheme to isolate protrusions and cell bodies from control or APC knockdown fibroblasts, which were induced to extend protrusions in response to addition of lysophosphatidic acid (LPA). Four replicate protrusion and cell body samples for each cell type were analyzed by RNA-Seq. To identify RNAs enriched in protrusions, a protrusion/cell body ratio was calculated. We find that ca. 7% of detected RNAs were enriched in protrusions of control cells. Knockdown of APC reduced the protrusion enrichement of a subset of these RNAs, indicating that they are dependent on APC for their localization. Localization of the remaining RNAs was not significantly affected upon APC knockdown suggesting that their localization is mediated by an APC-independent mechanism.
2017-10-11 | GSE82229 | GEO