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Transcriptome analysis of cultured human lung microvascular endothelial cells (HLMVECs) to explore functional roles for CD26/DPP4 in mediating inflammatory responses by LPS

ABSTRACT: Transcriptome analysis of cultured human lung microvascular endothelial cells (HLMVECs) to explore functional roles for CD26/DPP4 in mediating inflammatory responses by LPS

PROVIDER: PRJNA786946 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17161177.fastq.gz	Fastqsanger.gz
	SRR17161178.fastq.gz	Fastqsanger.gz
	SRR17161179.fastq.gz	Fastqsanger.gz
	SRR17161180.fastq.gz	Fastqsanger.gz
	SRR17161181.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcriptome analysis of cultured human lung microvascular endothelial cells (HLMVECs) to explore functional roles for CD26/DPP4 in mediating inflammatory responses by LPS

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.

2021-12-10 | GSE190405 | GEO

Transcriptome Analysis of Fibroblasts in Hypoxia-Induced Vascular Remodeling: Functional Roles of CD26/DPP4

Project description:In hypoxic pulmonary hypertension (PH), pulmonary vascular remodeling is characterized by the emergence of activated adventitial fibroblasts, leading to medial smooth muscle hyperplasia. Previous studies have suggested that CD26/dipeptidyl peptidase-4 (DPP4) plays a crucial role in the pathobiological processes in lung diseases. However, its role in pulmonary fibroblasts in hy-poxic PH remains unknown. Therefore, we aimed to clarify the mechanistic role of CD26/DPP4 in lung fibroblasts in hypoxic PH. Dpp4 knockout (Dpp4 KO) and wild-type (WT) mice were exposed to hypoxia for 4 weeks. The degree of PH severity and medial wall thickness was augmented in Dpp4 KO mice compared with that in WT mice, suggesting that CD26/DPP4 plays a suppressive role in the development of hypoxic PH. Transcriptome analysis of human lung fibroblasts cultured under hypoxic conditions revealed that TGFB2, TGFB3, and TGFA were all upregulated as differentially expressed genes after DPP4 knockdown with small interfering RNA treatment. These results suggest that CD26/DPP4 plays a suppressive role in TGFβ signal-regulated fibroblast ac-tivation under hypoxic conditions. Therefore, CD26/DPP4 may be a potential therapeutic target in patients with PH associated with chronic hypoxia.

2024-11-17 | GSE281533 | GEO

Transcriptome analysis of cultured human pulmonary artery smooth muscle cells (hPASMCs) to explore functional roles for CD26/DPP4 in stimulation with TGF-β1

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.

2024-01-03 | GSE248794 | GEO

Therapeutic Strategies for MMAE-Resistant Bladder Cancer Through DPP4 Inhibition

Project description:Monomethyl auristatin E (MMAE) is used as the cytotoxic payload for enfortumab vedotin (EV) in the treatment of locally advanced and metastatic bladder cancer (BC). However, the development of resistance to MMAE in BC is a therapeutic problem. To explore the mechanism of resistance to MMAE in BC, we established MMAE-resistant BC cells (MR-BCs). RNA sequencing analysis showed that the expression of dipeptidyl peptidase 4 (DPP4, also called CD26) increased significantly in MR-BCs compared with parental BC cells. Knock down of DPP4 expression using small interfering RNA inhibited the viability of MR-BCs. In addition, the DPP4 inhibitor sitagliptin suppressed the proliferation, migration, and invasion of BC cells, and cotreatment with MMAE effectively induced cell apoptosis, arrested cells in the G2M phase of the cell cycle, increased reactive oxygen species production by inhibiting the AKT pathway, and significantly inhibited the in vivo growth of MMAE-resistant cells. This study provides insights into the use of DPP4 inhibitors as a treatment strategy for MMAE-resistant BC.

2025-08-30 | GSE306410 | GEO

Transcriptome analysis of cultured human pulmonary artery smooth muscle cells (hPASMCs) to explore functional roles for CD26/DPP4 in stimulation with TGF-β1

Project description:Transcriptome analysis of cultured human pulmonary artery smooth muscle cells (hPASMCs) to explore functional roles for CD26/DPP4 in stimulation with TGF-β1

| PRJNA1046026 | ENA

Sheep dendritic cells CD26+ and CD26- versus total dendritic cells

Project description:Transcriptomic profiling of ovine skin lymph dendritic cell subsets CD26+ and CD26- compared to total enriched lymph dendritic cells. CD26+ and CD26- dendritic cells (DC) from sheep skin lymph were sorted by flow cytometry and were analysed for their transcriptomic profile. We demonstrate that the minor sheep CD26+ skin lymph DC subset shares significant transcriptomic similarities with mouse CD8a+ and human BDCA3+ DC. This allowed the identification of a common set of phenotypic characteristics for CD8a-like DC in the 3 mammalian species, i.e. SIRPlo, CADM1hi, CLEC9Ahi, DEC205hi, XCR1hi. Compared to CD26- DC, the sheep CD26+ DC show (1) potent stimulation of allogeneic naive CD8+ T cells with high selective induction of the Ifn-gamma and Il22 genes; (2) dominant efficacy in activating specific CD8+ T cells against exogenous soluble antigen; (3) selective expression of functional pathways associated to high capacity for antigen cross-presentation. Reference design (total enriched lymph dendritic cells) - Biological replicates: 2 sheep #10081 and #30066

2010-07-23 | E-GEOD-21889 | biostudies-arrayexpress

Transcriptome Analysis of Fibroblasts in Hypoxia-Induced Vascular Remodeling: Functional Roles of CD26/DPP4

Project description:Transcriptome Analysis of Fibroblasts in Hypoxia-Induced Vascular Remodeling: Functional Roles of CD26/DPP4

| PRJNA1184342 | ENA

Sheep dendritic cells CD26+ and CD26- versus total dendritic cells

2010-07-23 | GSE21889 | GEO

Mesothelioma cells: Control vs CD26 knockdown

Project description:CD26 is a prognostic factor in many cancers and implicated as therapeutic target. Knockdown of CD26 on mesothelioma cells H226 and JMN inhibit tumor progression. In order to elucidate CD26-mediated pathway for tumor progression, CD26 was knocked down on H226 and JMN cells, and RNAs from these cells were subjected to Microarray analysis.

2018-07-01 | GSE100241 | GEO

Functional Roles for CD26/DPP4 in Mediating Inflammatory Responses of Pulmonary Vascular Endothelial Cells.

Project description:Excessive inflammation in the lung is a primary cause of acute respiratory distress syndrome (ARDS). CD26/dipeptidyl peptidase-4 (DPP4) is a transmembrane protein that is expressed in various cell types and exerts multiple pleiotropic effects. We recently reported that pharmacological CD26/DPP4 inhibition ameliorated lipopolysaccharide (LPS)-induced lung injury in mice and exerted anti-inflammatory effects on human lung microvascular endothelial cells (HLMVECs), in vitro. However, the mechanistic roles of CD26/DPP4 in lung injury and its effects on HLMVECs remain unclear. In this study, transcriptome analysis, followed by various confirmation experiments using siRNA in cultured HLMVECs, are performed to evaluate the role of CD26/DPP4 in response to the pro-inflammatory involved in inflammation, barrier function, and regenerative processes in HLMVECs after pro-inflammatory stimulation. These are all functions that are closely related to the pathophysiology and repair process of lung injury. Confirmatory experiments using flow cytometry; enzyme-linked immunosorbent assay; quantitative polymerase chain reaction; dextran permeability assay; WST-8 assay; wound healing assay; and tube formation assay, reveal that the reduction of CD26/DPP4 via siRNA is associated with altered parameters of inflammation, barrier function, and the regenerative processes in HLMVECs. Thus, CD26/DPP4 can play a pathological role in mediating injury in pulmonary endothelial cells. CD26/DPP4 inhibition can be a new therapeutic strategy for inflammatory lung diseases, involving pulmonary vascular damage.

| S-EPMC8700481 | biostudies-literature

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