Effect of PDGF-Ddstimulation on human tonsil ILC1
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE107043 | GEO | 2018/02/01
REPOSITORIES: GEO
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Project description:Effect of PDGF-Ddstimulation on human tonsil ILC1
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Project description:Analysis of platelet-derived growth factor (PDGF)-stimulated fibroblasts. Results provide insight into novel pro-tumorigenic factors induced by PDGF-activation of fibroblasts. 1.2 x 10e6 BJ-hTERT fibroblasts were cultured in 10cm dish with Dulbecco's Modified Eagle Medium (DMEM; Gibco Life Technologies, Gergy-Pontoise, France) containing 1% heat-inactivated fetal calf serum (FCS), 2 mM L-glutamine, penicillin (100 units/ml) and streptomycin (100 ng/ml) at 37ºC in a 5% CO2 humidified atmosphere during 24h. Cultures were stimulated with or without 20ng/mL PDGF-BB (Peprotech, New Jersey, USA) for another 24h prior to harvest. Unstimulated fibroblasts were used as control samples. Cultures of both unstimulated and stimulated fibroblasts were done in triplicate.
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Project description:Human T98G glioblastoma cells were stimulated with platelet-derived growth factor (PDGF) and analyzed by DNA microarrays, which identified 74 immediate-early gene transcripts. Cells were then treated with inhibitors to identify subsets of genes that are targets of the phosphatidylinositol 3-kinase (PI3K) and MEK/ERK signaling pathways. Four groups of PDGF-induced genes were defined: independent of PI3K and MEK/ERK signaling, dependent on PI3K signaling, dependent on MEK/ERK signaling, and dependent on both pathways. Cells were grown in Minimal Essential Medium (Invitrogen) supplemented with fetal calf serum (10%). For growth factor/inhibitor treatments, cells were incubated in serum-free medium for 72 h, and either left unstimulated, or stimulated for 30 min with human PDGF-BB (50 ng/ml) (Sigma). U0126 (Cell Signaling Technology) and LY294002 (BioMol) were added 60 min prior to PDGF addition. Keywords: other
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Project description:Obesity-induced secretory disorder of adipose tissue-derived factors is important for cardiac damage. However, whether platelet-derived growth factor-D (PDGF-D), a newly identified adipokine, regulates cardiac remodeling in Angiotensin II (AngII)-infused obese mice is unclear. Here, we found obesity induced PDGF-D expression in adipose tissue, as well as more severe cardiac remodeling compared to control lean mice after AngII infusion. Adipocyte-specific PDGF-D knockout attenuated hypertensive cardiac remodeling in obese mice. Consistently, adipocyte-specific PDGF-D overexpression transgenic mice (PA-Tg) showed exacerbated cardiac remodeling after AngII infusion without high-fat diet treatment. Mechanistic studies indicated that AngII-stimulated macrophages produce urokinase plasminogen activator (uPA) that activates PDGF-D by splicing full-length PDGF-D into the active PDGF-DD. Moreover, bone marrow specific uPA knockdown decreased active PDGF-DD level in the heart and improved cardiac remodeling in HFD hypertensive mice. Together, our data provide for the first time a new interaction pattern between macrophage and adipocyte, that macrophage-derived uPA activates adipocyte-secreted PDGF-D, which finally accelerates AngII-induced cardiac remodeling in obese mice.
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Project description:This experiment tests the hypothesis that interleukin-1 promotes SMC phenotypic modulation to a distinct inflammatory state relative to the growth factor PDGF-DD. Cultured rat aortic smooth muscle cells were treated with IL-1b (2.5 ng/mL) or vehicle (0.1% BSA and 10 mM acetic acid) or PDGF-DD (30 ng/mL) or vehicle (0.01% BSA) for 24 hours prior to harvest (n=1).
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Project description:This experiment tests the hypothesis that interleukin-1 promotes SMC phenotypic modulation to a distinct inflammatory state relative to the growth factor PDGF-DD.
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