Transcriptome analysis of cultured human lung microvascular endothelial cells (HLMVECs) to explore functional roles for CD26/DPP4 in mediating inflammatory responses by LPS
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PROVIDER: PRJNA786946 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: The purpose of this study is to evaluate the role of CD26/DPP4 in HLMVECs in response to the pro-inflammatory stimulus LPS. Methods: Four primary cell lines of HLMVECs were used. HLMVECs were cultured in endothelial growth medium-2 supplemented with 10% fetal bovine serum. The cells were incubated at 37°C in a 5% CO2 incubator and used at passages 6–8 for all experiments. 2 kinds of CD26/DPP4 siRNA were used. HLMVECS were treated with CD26/DPP4 siRNA or non-specific control siRNA or vehicle for 72 hours, then stimulated with LPS or PBS for 18 hours. Results: Varieties of DEGs were determined between groups leading to the enrichment analysis. Conclusions: The results suggest that CD26/DPP4 expression is related to multiple important functions in HLMVECs, including inflammation, barrier function, and regenerative processes.
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Project description:The purpose of this study was to evaluate the role of CD26/DPP4 in hPASMCs in response to TGF-β1. In experimental methods, hPASMCs were treated as follows. The hPASMCs were cultured in Smooth Muscle Cell Growth Medium 2 with 10% fetal bovine serum and were incubated at 37 ℃ in a 5% CO2 incubator. The cells at passage 6 were used for all experiments. The PASMCs were treated with CD26/DPP4 siRNA or non-specific control siRNA for 48 hours, then stimulated with TGF-β1 or PBS for 24 hours. Transcriptome analysis revealed that TGFβ treatment in cultured hPASMCs upregu-lated genes related to pulmonary vascular SMC proliferation, involving the Notch, PI3K-Akt, and NFκB signaling pathways.Conversely, DPP4-siRNA treatment in cultured hPASMCs downregulated these pathways.
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Project description:Transcriptional profiling of primary human white preadipocytes after infection with lentiviral vector either containing shRNA directed against dipeptidypeptidase 4 (DPP4) or unspecific shRNA as negative control Treatment of cells with DPP4 shRNA or control shRNA was done in 4 biological replicates, the first sample of DPP4 KD was hybridized against the first sh-control sample, the second DPP4 smple against the second control sample and so on
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Project description:We performed scRNA sequencing to understand the composition and differential gene expression changes in aortic cells from LDLR-/- mice fed a normal diet (ND), high-fat diet (HFD), or HFD + DPP4i. We combined this technique with CITE-sequencing to measure the cell surface protein expression (DPP4) and transcriptomic changes associated with our experimental conditions as well as changes associated with DPP4 cell surface expression in all aortic cells.
2023-05-18 | GSE209525 | GEO
Project description:Elevated circulating dipeptidyl-peptidase 4 (DPP4) is a biomarker for liver disease, but its involvement in gluconeogenesis and metabolic associated fatty liver disease (MAFLD) progression remains unclear. Here we identified that DPP4 in hepatocytes but not Tie2+ endothelial cells regulates the local bioactivity of incretin hormones and gluconeogenesis. However, the complete absence of DPP4 (Dpp4-/-) in aged mice with metabolic syndrome accelerates liver fibrosis without altering dyslipidemia and steatosis. Analysis of transcripts from the livers of Dpp4-/- mice displayed enrichment for inflammasome, p53, and senescence programs compared to littermate controls. High-fat high-cholesterol (HFHC)-feeding decreased Dpp4 expression in F4/80+ cells, with only minor changes in immune signaling.
2023-01-31 | GSE218765 | GEO
Project description:Elevated circulating dipeptidyl-peptidase 4 (DPP4) is a biomarker for liver disease, but its involvement in gluconeogenesis and metabolic associated fatty liver disease (MAFLD) progression remains unclear. Here we identified that DPP4 in hepatocytes but not Tie2+ endothelial cells regulates the local bioactivity of incretin hormones and gluconeogenesis. However, the complete absence of DPP4 (Dpp4-/-) in aged mice with metabolic syndrome accelerates liver fibrosis without altering dyslipidemia and steatosis. Analysis of transcripts from the livers of Dpp4-/- mice displayed enrichment for inflammasome, p53, and senescence programs compared to littermate controls. High-fat high-cholesterol (HFHC)-feeding decreased Dpp4 expression in F4/80+ cells, with only minor changes in immune signaling.
2023-01-31 | GSE218766 | GEO
Project description:Skin-injury and several diseases elicit fibrosis and induce hair follicle (HF)-growth arrest and loss. Resulting alopecia and disfiguration represent a severe burden for patients both physically and psychologically. Reduction of pro-fibrotic factors such as DPP4 might be a strategy to tackle this issue. We demonstrate DPP4-overrepresentation in settings with HF-growth arrest (telogen), HF-loss and non-regenerative wound areas in mice skin and human scalp. Topical DPP4-inhibition (DPP4i) with FDA/EMA-approved Sitagliptin (Sit) on preclinical models of murine HF-activation/regeneration results in accelerated anagen-progress, while treatment of wounds with Sit results in reduced expression of fibrosis markers, increased induction of anagen around wounds, and HF-regeneration in the wound center. These effects are associated with higher expression of Wnt-target Lef1, known to be required for HF-anagen (HF-activation)/regeneration. Sit-treatment decreases pro-fibrotic signaling in the skin, induce a differentiation trajectory of HF-cells, and activate Wnt-targets related to HF-activation/growth but not those supporting fibrosis. Taken together, our study demonstrates a role for DPP4 in HF biology and shows how DPP4i, currently used as oral medication to treat diabetes, could be repurposed into a topical treatment agent to potentially reverse HF-loss in alopecia and after injury.
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