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The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis [MeDIP-seq]

ABSTRACT: The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis [MeDIP-seq]

PROVIDER: PRJNA498092 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8098463_1.fastq.gz	Fastqsanger.gz
	SRR8098463_2.fastq.gz	Fastqsanger.gz
	SRR8098464_1.fastq.gz	Fastqsanger.gz
	SRR8098464_2.fastq.gz	Fastqsanger.gz
	SRR8098465_1.fastq.gz	Fastqsanger.gz

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The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis [MeDIP-seq]

Project description:Transforming growth factor‐beta (TGF‐β1) plays an important regulatory role in the progression of chronic kidney failure. Further, damage to kidney glomerular mesangial cells is central to the progression of diabetic nephropathy. The aim of this study was to explore the genetic associations between mRNA, microRNA, and epigenetics in mesangial cells in response to TGF‐β1. The regulatory effects of TGF‐β1 on mesangial cells were investigated at different molecular levels by treating mesangial cells with TGF‐β1 for 3 days followed by genome‐wide miRNA, RNA, MeDIP-seq, and H3K27Me3 expression profiling using next-generation sequencing (NGS). Each sample was designed with 3 repeat samples.

2018-10-24 | GSE121687 | GEO

The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis [miRNA-seq]

2018-10-24 | GSE121701 | GEO

The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis [RNA-seq]

2018-10-24 | GSE121700 | GEO

The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis [H3K27me3 ChIP-seq]

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Transcriptomic Changes in TGF-β1 Differentiated and PGE2 Dedifferentiated Myofibroblasts

Project description:These data show that the genes that distinguish myofibroblasts from fibroblasts are myriad, and that some genes not traditionally associated with myofibroblast differentiation may serve as novel therapeutic targets for fibrosing disorders. Gene expression levels were assessed from total RNA on the Affymetrix U219 microarray. Here, we use transforming growth factor-β1 (TGF-β1) and prostaglandin E2 (PGE2), which has recently been shown to reverse myofibroblast differentiation, to investigate the transcriptomic changes that occur during TGF-β1-induced differentiation and PGE2-induced de-differentiation of myofibroblasts.

2015-06-30 | E-GEOD-63659 | biostudies-arrayexpress

The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis

Project description:The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis

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A mRNA motif mediates TGF-β1 upregulation of NEU3 translation in human lung fibroblasts

Project description:To elucidate how TGF-β1 regulates translation, we treated human lung fibroblasts (HLF) with TGF-β1 and used RNA-seq to determine the effect of TGF-β1 on total RNAs, and mRNA polysome/monosome ratios.

2022-04-28 | GSE201506 | GEO

The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis [miRNA-seq]

Project description:The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis [miRNA-seq]

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The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis [RNA-seq]

Project description:The use of targeted next-generation sequencing to determine the regulatory function of TGF‐β1 in kidney fibrosis [RNA-seq]

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TGF-β1 activates neutrophil signaling and transcription but not migration

Project description:Tumor-associated neutrophils are found in many types of cancer and are often reported to contribute to negative outcomes. Several studies have shown that the presence of TGF-β in the tumor microenvironment contributes to the skewing of neutrophils to have a more pro-tumor phenotype. However, the direct effects of TGF-β on neutrophil signaling and migration are unclear. We sought to characterize TGF-β signaling in both primary human neutrophils and the neutrophil-like cell line HL-60 and determine whether TGF-β directly induces neutrophil migration. We found that TGF-β1 does not induce neutrophil migration in either a transwell or an underagarose migration assay. However, TGF-β1 does activate signals canonically through SMAD3 and noncanonically through ERK1/2 in neutrophils in a time and dose-dependent manner. Additionally, TGF-β1 present in the tumor-conditioned media (TCM) is responsible for SMAD3 activation. Moreover, we discovered that TCM from aggressive breast cancer cells induces neutrophils to secrete leukotriene B4 (LTB4), which is a lipid mediator important for amplifying neutrophil recruitment. However, we found that TGF-β1 alone does not induce secretion of LTB4. We next performed RNA-sequencing to evaluate the effects of TGF-β1 and TCM on the neutrophil transcriptome. We found that TGF-β1 and TCM result in changes in gene transcription in HL-60 cells, specifically of two pro-tumor genes OSM and VEGFA. Together, our findings characterize the effects of TGF-β1 on neutrophil signaling, migration, and gene expression that can be applied to understanding the changes in neutrophils that occur in the tumor microenvironment.

2023-08-10 | GSE230490 | GEO

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