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Hypermethylation leads to the loss of HOXA5, resulting in JAG1 expression and NOTCH signaling for renal fibrosis

ABSTRACT: Hypermethylation leads to the loss of HOXA5, resulting in JAG1 expression and NOTCH signaling for renal fibrosis

PROVIDER: PRJNA1032906 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26551565_1.fastq.gz	Fastqsanger.gz
	SRR26551565_2.fastq.gz	Fastqsanger.gz
	SRR26551566_1.fastq.gz	Fastqsanger.gz
	SRR26551566_2.fastq.gz	Fastqsanger.gz
	SRR26551567_1.fastq.gz	Fastqsanger.gz

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Hypermethylation leads to the loss of HOXA5, resulting in JAG1 expression and NOTCH signaling for renal fibrosis

Project description:DNA methylation has been implicated in renal fibrosis. In this study, we demonstrated the induction of DNA methyltransferases and global DNA methylation in fibrotic kidneys, and further proved the beneficial effects of their inhibitor 5-Aza in renal fibrosis. HOXA5 was shown to be down-regulated in fibrotic kidneys through hypermethylation, and this down-regulation led to JAG1 expression and consequent activation of NOTCH signaling for renal fibrogenesis. These findings unveil DNA methylation and related genes, such as HOXA5, as potential therapeutic targets in renal fibrotic disease.

2023-11-27 | GSE246417 | GEO

JAG1 Mediated Notch Signaling Regulates Secretory Cell Differentiation of the Human Airway Epithelium

Project description:Background: Basal cells (BC) are the stem/progenitor cells of the human airway epithelium capable of differentiating into secretory and ciliated cells. Notch signaling activation increases BC differentiation into secretory cells, but the role of individual Notch ligands in regulating this process is unknown Results: The objective of this study was to define the role of the Notch ligand JAG1 in regulating BC differentiation. JAG1 over-expression in BC increased secretory cell differentiation, with no effect on ciliated cell differentiation. Conversely, knockdown of JAG1 decreased expression of secretory cell genes. Conclusions: These data demonstrate JAG1 mediated Notch signaling regulates differentiation of BC into secretory cells. This study demonstrates that expression of the Notch ligand JAG1 is highly enriched in basal stem/progenitor cells (BC) of the human airway epithelium and that modulation of its expression levels during differentiation of BC play an important role in regulating secretory cell differentiation with no effect on ciliated cell differentiation. These observations have implications for developing novel targets to specifically modulate levels of secretory cells in human airway disorders.

2017-08-23 | GSE76421 | GEO

Notch engagement by Jag1 clusters on the nanoscale suggests a force-independent mode of activation

Project description:The Notch signaling pathway is a cell-cell communication system with fundamental roles in embryonic development and the nervous system, including neural stem cell proliferation and differentiation. To investigate the multivalency effect of ligands on the activation of the Notch receptor, we treated iPSc-derived neuroepithelial stem-like (lt-NES) cells with different Jag1 nanopatterns on DNA origami nanostructures.

2023-11-23 | E-MTAB-12439 | biostudies-arrayexpress

The role HOXA5 in extrahepatic cholangiocarcinoma (Methylation)

Project description:Homeobox A5 (HOXA5) is a transcription factor in mammalian and can regulate cell differentiation, proliferation and apoptosis as well as tumorigenesis. However, little is known on whether and how HOXA5 can regulate the malignant behaviors of cholangiocarcinoma. The methylation levels of HOXA5 were evaluated by methylation microarray and bisulfite sequencing PCR. We found that hypermethylation in the HOXA5 promoter down-regulated HOXA5 expression in extrahepatic cholangiocarcinoma (ECCA) tissues, which was correlated with worse overall survival. HOXA5 over-expression significantly inhibited the proliferation and tumor growth.

2022-10-05 | GSE211911 | GEO

Transcription profiling of human endometrial stromal cells to idenify Jag1-dependent gene expression

Project description:The goal is to investigate gene regulation in endometrial stromal cells expressing the Notch ligand Jag1. Experiment Overall Design: This study compares gene expression in Jag1 retrovirus-infected and control (empty virus-infected) stromal cells.

2009-07-11 | E-GEOD-16906 | biostudies-arrayexpress

JAG1-NOTCH4 mechanosensing drives atherosclerosis

Project description:Endothelial cell (EC) sensing of fluid shear stress regulates atherosclerosis, a disease of arteries that causes heart attack and stroke. Atherosclerosis preferentially develops at regions of arteries exposed to low oscillatory shear stress (LOSS), whereas high shear regions are protected. We show using inducible EC-specific genetic deletion in hyperlipidaemic mice that the Notch ligands JAG1 and DLL4 have opposing roles in atherosclerosis. While endothelial Jag1 promoted atherosclerosis at sites of LOSS, endothelial Dll4 was atheroprotective. Analysis of porcine and murine arteries and cultured human coronary artery EC exposed to experimental flow revealed that JAG1 and its receptor NOTCH4 are strongly upregulated by LOSS. Functional studies in cultured cells and in mice with EC-specific deletion of Jag1 show that JAG1-NOTCH4 signalling drives vascular dysfunction by repressing endothelial repair. These data demonstrate a fundamental role for JAG1-NOTCH4 in sensing LOSS during disease, and suggest therapeutic targeting of this pathway to treat atherosclerosis.

2022-09-06 | GSE206117 | GEO

Jag1-dependent gene expression in human endometrial stromal cells

Project description:The goal is to investigate gene regulation in endometrial stromal cells expressing the Notch ligand Jag1.

2009-07-01 | GSE16906 | GEO

Transcriptomes of control and JAG1-deficient cochlea

Project description:The aim of this study is to identify the gene targets of the Notch ligand JAG1 in the postnatal cochlea. JAG1 was conditionally deleted in mice carrying both an inducible Cre allele (Sox2CreER) and a floxed (fl) Jag1 allele. Tamoxifen was administered to P0/P1 pups. Cochlear tissues from 6 Sox2CreER/+Jag1fl/fl and wildtype littermate controls were dissected under the dissecting microscope in ice-cold DEPC-treated PBS and stored in RNAlater (Invitrogen) at 4C. The RNAs were purified by RNeasy Micro Kit (QIAGEN). The quality and quantity of RNAs were measured by a 2100 bioanalyzer (Agilent). Illumina compatible sequencing libraries were generated by the University of Rochester Genomics Research Center. Libraries were hybridized to the Illumina flow cell and single-end reads of 100nts were generated. Identification of significantly differentially expressed genes was determined using DeSeq2. We found 548 differentially expressed genes with an adjusted p-value of <0.05, 411 of those genes were significantly upregulated while 137 were significantly downregulated. Analysis of pathways revealed novel genes involved downstream of JAG1-Notch signaling in the postnatal cochlea.

2022-12-09 | GSE193158 | GEO

Transcription profiling of human LEC cells reveals KSHV manipulates notch signaling by upregulating Dll4 and JAG1 to alter cell cycle gene expression in

Project description:Kaposi sarcoma is the most common cancer in AIDS patients and is typified by red skin lesions. The disease is caused by the KSHV virus (HHV8) and is recognizable by its distinctive red skin lesions. The lesions are KSHV infected spindle cells, most commonly the lymphatic endothelial and blood vessel endothelial cells (LEC and BEC), plus surrounding stroma. Here we examine KSHVs modulation of Notch signaling using wild-type LEC cells co-cultured with DLL4 and JAG1 expressing LEC cells. Experiment Overall Design: There are 1) n=2 of LEC control cells co-cultured with pSIN expressing LEC, 2) n=3 of LEC co-cultured with pSIN-Dll4 expressing LEC, and 3) n=3 of LEC co-cultured with pSIN-JAG1 expressing LEC.

2009-12-05 | E-GEOD-16547 | biostudies-arrayexpress

JAG1-NOTCH4 mechanosensing drives atherosclerosis [single-cell RNA-seq]

2022-09-06 | GSE207275 | GEO