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Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (mRNA-Seq)

ABSTRACT: Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (mRNA-Seq)

PROVIDER: PRJNA980670 | ENA |

REPOSITORIES: ENA

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Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling.

Project description:Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling.

| PRJNA980665 | ENA

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (Spatial Gene Expression)

Project description:Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (Spatial Gene Expression)

| PRJNA980674 | ENA

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (single cell RNA-Seq)

Project description:Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (single cell RNA-Seq)

| PRJNA980671 | ENA

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling.

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-09-30 | GSE234272 | GEO

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (mRNA-Seq)

Project description:To elucidate the molecular mechanisms underlying the roles of inflammatory cells in scar formation, we performed RNA-seq of inflammation-related mRNAs and miRNAs from both wild-type mice and PU.1 knock-out mice (PU.1 KO). This approach allowed us to comprehensively investigate how inflammation-related gene expression influences the skin wound healing process.

2024-09-30 | GSE234270 | GEO

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (Spatial Gene Expression)

Project description:Spatial transcriptome analysis (Visium, 10x Genomics) was performed to define the spatial topography of inflammation-related gene expressions in microenvironments of wound tissues.

2024-09-30 | GSE234271 | GEO

Novel integrated multiomics analysis reveals Itgbl1-mediated regulation of fibrogenesis through antagonism of Tgfβ1 and IL1β signaling. (single cell RNA-Seq)

Project description:To understand the molecular mechanism of minority cell population in skin would healing process, we performed single cell RNA sequencing (scRNA-seq) of murine skin wound tissues at 3 different time points after injury (3d, 7d, 14d).

2024-09-30 | GSE234269 | GEO

Gene expression profiles associated with ITGBL1 overexpression

Project description:In our previous microarray study we identified two subgroups of high-grade serous ovarian cancers with distinct gene expression and different survival. Among differentially expressed genes was an Integrin beta-like 1 (ITGBL1), coding for a poorly characterized protein comprised of ten EGF-like repeats. In this study we investigated ITGBL1 influence on ovarian cancer cells phenotype. Using various functional assays we found that ITGBL1 overexpression affected cellular adhesion, migration and invasiveness, while it had no effect on proliferation rate and the cell cycle. ITGBL1-overexpressing cells were significantly more resistant to cisplatin and paclitaxel, major drugs used in ovarian cancer treatment. Global gene expression analysis revealed that signaling pathways affected by ITGBL1 overexpression were mostly those related to extracellular matrix organization and function, integrin signaling, focal adhesion, cellular communication and motility; these results were consistent with the findings of our functional studies. Overall, our results indicate that higher expression of ITGBL1 in ovarian cancer is associated with features that may worsen clinical course of the disease.

2021-02-03 | GSE166029 | GEO

miR548ai antagonism attenuates exosome-induced endothelial cell dysfunction

Project description:We performed microarray profiling of microRNAs of dysfunctional human primary aortic SMCs induced by different cytokines (PDGF-BB, TGFβ1, TNFα, IL1β).

2021-11-03 | GSE185784 | GEO

A master cistromic circuit governing hepatic fibrogenesis [ChIP-seq]

Project description:Liver fibrosis is a reversible wound-healing response to liver injury and hepatic stellate cells (HSCs) are central cellular players that mediate hepatic fibrogenesis. However, the molecular mechanisms that govern this process remain unclear. Here, we reveal a novel cistromic circuit in HSCs comprising the vitamin D receptor (VDR) and SMAD transcription factors that restrains the intensity of hepatic fibrogenesis. Ligand-activated VDR suppresses TGFβ1-induced pro-fibrotic gene expression in HSCs. Administration of a vitamin D analogue, calcipotriol, diminishes the fibrotic response in a mouse model of liver fibrosis, while VDR knockout mice spontaneous develop extensive hepatic fibrosis by age 6 months. Using ChIP-Seq, we find that the anti-fibrotic properties of VDR are due to crosstalk with SMAD, mediated by their co-occupancy of DNA-binding sites on pro-fibrotic genes. Specifically, SMAD binding potentiates local chromatin accessibility to enhance VDR recruitment at the same cis-regulatory elements, which reciprocally antagonizes the interaction between SMAD3 and chromatin and limits the assembly of transcriptional activation complexes at fibrotic genes, a process that is enhanced by the presence of VDR agonists. These results not only establish this coordinated VDR/SMAD cistromic circuit as a master regulator of hepatic fibrogenesis, but also support VDR as a potential drug target to ameliorate liver fibrosis. Identification of VDR, SMAD3 and H3 binding sites in human stellate LX2 cells that were pre-treated with calcipotriol (100nM) for 16 hrs (where calcipotriol treatment is indicated) followed by incubation of calcipotriol (100nM) or TGFβ1 (1ng/ml) for another 4 hours (where indicated).

2013-04-29 | E-GEOD-38103 | biostudies-arrayexpress

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