Human gingival fibroblasts: control vs. lysophosphatidic acid (LPA 18:1)-treated
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: D. Cerutis
PROVIDER: E-GEOD-57496 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:LPA, which can signal through the Ga12/13 family of G proteins, is a potent stimulator of fibroblast migration. LPA downregulate mTOR activity dependent on protein synthesis in cell migration and bleomycin-induced lung fibrosis. We used microarray to identify LPA-regualted gene expression and find potent regulators in this process. HEK293 cells were treated with or without LPA. Then RNA was extracted and Hybridization was done on Affymetrix microarrays.
2012-01-14 | E-GEOD-35084 | biostudies-arrayexpress
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-miRNA expression profile in human breast cancer cell lines MDA-MB-231 MDA-MB-231 cells were serum starved for 24h and then stimulated with LPA (1µM) for 45min. The controls were the serum starved unstimulated cells. Three replicates were included in this study.
2015-05-05 | E-GEOD-64100 | biostudies-arrayexpress
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
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) MDA-MB-231, MCF7, PC3 cells were serum starved for 24h and then stimulated with LPA (1µM) for 45min. The controls were the serum starved unstimulated cells. Two replicates for each sample were included in this study. Microarray analysis was performed using a high-density oligonucleotide array (GeneChip Human Genome U133 plus 2.0 array, Affymetrix)
2014-05-16 | E-GEOD-56265 | 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:Multilineage-differentiating stress enduring (Muse) cells are nontumorigenic endogenous pluripotent-like stem cells easily collected from various adult or fetal tissues. The tissue regenerative effects of Muse cells have been demonstrated in many disease models, as they reach damaged sites after intravenous injection to exert pleiotropic effects. Previous reports indicate that several human tissues are readily accessible for Muse cell isolation, including adult tissues such as bone marrow (BM) and embryonic tissues such as Wharton’s Jelly (WJ) from umbilical cord. Wa analyzed the protein repertoires of WJ-Muse and BM-Muse using mass spectrometry-based proteomics.
2023-07-17 | PXD036883 | Pride
Project description:Brown adipose tissue (BAT) is a thermogenic organ that dissipates stored energy as heat to maintain body temperature in infants and small mammals. This process may also provide protection from development of diet-induced obesity. We found that the bioactive lipid mediator lysophosphatidic acid (LPA) markedly decreases differentiation of cultured primary brown adipocyte precursors, while potent selective inhibitors of the LPA-generating enzyme autotaxin (ATX) promote differentiation. Transgenic mice overexpressing ATX exhibited reduced expression of BAT-related genes in peripheral white adipose tissue and accumulated significantly more fat than wild-type controls when fed a high fat diet. Our results indicate that ATX and its product LPA are physiologically relevant negative regulators of brown fat adipogenesis and suggest that a decrease in peripheral brown adipose tissue results in increased susceptibility to diet-induced obesity in mice. Primary BAT cell cultures were established as previously reported with some minor modifications (Cannon B., 2001; Néchad M., 1983). Four- to 6-week-old mice were euthanized under aseptic conditions and interscapular BAT (IBAT) dissected, finely minced in digestion buffer containing 123 mM NaCl, 5mM HCl, 1.3 mM CaCl2, 5mM glucose, 1.5% (w/v) crude bovine serum albumin fraction V, 100 mM HEPES, 0.2% collagenase type II (Sigma-Aldrich Corp., St. Louis, MO), pH 7.4, and digested in 10 ml of the same buffer for 30 min at 37°C. The supernatant obtained was then filtered using a 250 µm nylon mesh and kept in ice for 15 minutes to allow fat droplets and mature cells to float. The resulting infranatant was filtered through a 30 µm nylon mesh to enrich the fraction with precursor cells and centrifuged at 700g for 10 min. The pellet obtained was washed once in warm DMEM and resuspended in DMEM medium containing 10% newborn calf serum, 10 mM HEPES, 4mM glutamine, 25 µg/ml sodium ascorbate (Sigma-Aldrich Corp., St. Louis, MO)., 100U/ml penicillin and 100mg/ml streptomycin. Cells were seeded onto 35mm dish plates. Insulin treatment was started on day 1 at 50 nM and the concentration increased to 100 nM at day 5 and 200 nM at day 7. Differentiated/confluent cells were collected for biochemical analysis (~day 9). To identify genes regulated by ATX and LPA signaling, 9 DIV primary BAT cultures were treated with the vehicle (DMSO), specific ATX inhibitor HA155 (2.5µM), or LPA (1-Oleoly-LPA, 5µM) (Avanti Polar Lipids, AL, USA) during differentiation. Treatment of the BAT cultures did not affect confluence or markers of proliferation. RNA was extracted from three cultures per condition using TRIzol reagent (Invitrogen, Carlsbad, CA) as described previously (Blalock EM., 2003).
2011-06-01 | E-GEOD-26442 | biostudies-arrayexpress
Project description:Pancreatic ductal adenocarcinoma is one of the most invasive and metastatic cancers and has a dismal 5-year survival rate. Here we show that N-WASP is required for the metastatic process, with roles in both chemotaxis, steering cells out of primary tumours, and matrix remodelling, allowing them to escape. Lysophosphatidic acid, a signalling lipid abundant in blood and ascites fluid, is both a mitogen and chemoattractant for PDAC cells. Pancreatic cancer cells efficiently break LPA down as they respond to it, setting up a self-generated gradient that directs cells out of the tumour. N-WASP depleted cells are unable to respond to LPA gradients and show altered RhoA activation, leading to a loss of cell contractility and traction forces, and reduced metastasis in vitro and in vivo. N-WASP couples LPA receptor signalling to RhoA via the endocytic adapter SNX18, and promotes sensitivity by preventing receptor degradation and promoting recycling of the LPA receptor back to the cell surface. Coordinated by N-WASP, the LPA-LPAR signalling loop promotes RhoA-mediated contractility and force generation. Perturbing this pathway chemically, or by CRISPR deletion severely impairs invasion through complex 3D environments or peritoneal explants, and impairs remodelling of fibrillar collagen. We thus reveal N-WASP as a central controller of a chemotactic loop between PDAC cells and microenvironmental conditions that drives metastasis.
2020-03-06 | PXD014506 | Pride
Project description:Physiological stimuli such as thrombin or pathological stimuli such as lysophosphatidic acid (LPA) activate platelets. The activated platelets bind to monocyte through P-selectin-PSGL-1 interactions, but also release the contents of their granules, which were defined as platelet releasate. It is known that monocytes in contact with platelet releasate produce reactive oxygen species (ROS). Reversible cysteine oxidation by ROS has been viewed as a potential regulator of protein function. In previous study, we employed a model of THP-1 monocytic cells affected by LPA- or thrombin-induced platelet releasate and a modified biotin switch assay to unravel the biological processes that been influenced by reversible cysteine oxidation. To gain better understanding of the redox regulation of monocyte in atherosclerosis, we now extend the modified biotin switch to quantify protein sulfenic acid, a subpopulation of reversible cysteine oxidation. Using arsenite in the modified biotin-switch assay, we were able to quantify 1161 proteins, in which more than 100 sulfenic acid sites were identified. Bioinformatics analysis of the quantified sulfenic acid sites further highlighted biological processes of monocyte transendothelial migration including integrin β2. Flow cytometry validated the activation of LFA-1 (αLβ2) and Mac-1 (αMβ2), two subfamilies of integrin β2 complexes on human primary monocyte upon platelet releasate treatments. The activation of LFA-1 was mediated by ROS from NADPH oxidase (NOX) activation. Moreover, the production of ROS and the activation of LFA-1 in human primary monocyte induced by platelet releasate were independent of P-selectin-PSGL-1 interaction. The modified biotin switch assay proved to be a powerful tool with the ability to reveal new regulatory mechanisms and identify new therapeutic targets.
2016-10-10 | PXD003363 | Pride
Project description:Physiological stimuli such as thrombin or pathological stimuli such as lysophosphatidic acid (LPA) activate platelets. The activated platelets bind to monocyte through P-selectin-PSGL-1 interactions, but also release the contents of their granules, which were defined as platelet releasate. It is known that monocytes in contact with platelet releasate produce reactive oxygen species (ROS). Reversible cysteine oxidation by ROS has been viewed as a potential regulator of protein function. In previous study, we employed a model of THP-1 monocytic cells affected by LPA- or thrombin-induced platelet releasate and a modified biotin switch assay to unravel the biological processes that been influenced by reversible cysteine oxidation. To gain better understanding of the redox regulation of monocyte in atherosclerosis, we now extend the modified biotin switch to quantify protein sulfenic acid, a subpopulation of reversible cysteine oxidation. Using arsenite in the modified biotin-switch assay, we were able to quantify 1161 proteins, in which more than 100 sulfenic acid sites were identified. Bioinformatics analysis of the quantified sulfenic acid sites further highlighted biological processes of monocyte transendothelial migration including integrin β2. Flow cytometry validated the activation of LFA-1 (αLβ2) and Mac-1 (αMβ2), two subfamilies of integrin β2 complexes on human primary monocyte upon platelet releasate treatments. The activation of LFA-1 was mediated by ROS from NADPH oxidase (NOX) activation. Moreover, the production of ROS and the activation of LFA-1 in human primary monocyte induced by platelet releasate were independent of P-selectin-PSGL-1 interaction. The modified biotin switch assay proved to be a powerful tool with the ability to reveal new regulatory mechanisms and identify new therapeutic targets.
2016-10-10 | PXD003365 | Pride