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Functional blockade of α5β1 integrin induces scattering and genomic landscape remodeling of hepatic progenitor cells

ABSTRACT: Cells treated with a specific antibody against α5β1 integrin exhibited cell spreading and scattering, over-expression of liver stem/progenitor cell markers and activation of the ERK1/2 and p38 MAPKs signaling cascades, in a similar manner to the process triggered by HGF/SF1 stimulation. Gene expression profiling revealed marked transcriptional changes of genes involved in cell adhesion and migration, as well as genes encoding chromatin remodeling factors. These responses were accompanied by conspicuous spatial reorganization of centromeres, while integrin genes conserved their spatial positioning in the interphase nucleus. Untreated cells versus HGF/SF1 treated or α5β1 integrin-mediated cell migration

ORGANISM(S): Mus musculus

SUBMITTER: Rune Matthiesen

PROVIDER: E-GEOD-23853 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Functional blockade of α5β1 integrin induces scattering and genomic landscape remodeling of hepatic progenitor cells

Project description:Cells treated with a specific antibody against α5β1 integrin exhibited cell spreading and scattering, over-expression of liver stem/progenitor cell markers and activation of the ERK1/2 and p38 MAPKs signaling cascades, in a similar manner to the process triggered by HGF/SF1 stimulation. Gene expression profiling revealed marked transcriptional changes of genes involved in cell adhesion and migration, as well as genes encoding chromatin remodeling factors. These responses were accompanied by conspicuous spatial reorganization of centromeres, while integrin genes conserved their spatial positioning in the interphase nucleus.

2010-08-27 | GSE23853 | GEO

Gene expression profiling of SF1 in mouse uterus tissues

Project description:Epigenetic silencing of Steroidogenic Factor 1 (SF1) is lost in endometrial tissue in endometriosis and this is hypothesized to result in de novo local steroidogenesis favoring growth and inflammation. The goal of this study was to evaluate the endometrial specific transcriptional and functional role of SF1 in vivo by utilizing a mouse model in which SF1 was conditionally expressed in the uterus. SF1 expression resulted in the development of cystic endometrial glands and infertility. Endometriosis induction by auto-transplantation of a biopsy of uterine tissue sutured to the mesenteric membrane resulted in 4-fold increase in size ectopic lesions from SF1 expressing mice. Microarray analysis demonstrated SF1-regulated genes are involved in several pathways including epithelial and tube development, migration of lymphocytes and leukocytes, cellular movement and vascular development. experimental group (SF-1 transgenic) and control group

2016-04-14 | E-GEOD-66963 | biostudies-arrayexpress

Gonadal Identity in the Absence of pro-Testis Factor SOX9 and pro-Ovary Factor beta-catenin

Project description:The main goal of our study is to identify the molecular events that determine the gonadal identity in mammals. Although testis and ovary arise from a common embryonic primordium, they represent outcomes of opposing fate determination. This decision to differentiate into a testis or an ovary hinges upon the balance between two antagonizing factors, pro-testis SOX9 and pro-ovary β-catenin. This microarray analysis led to the identification of the genes involved in the fate of XX and XY gonads in absence of SOX9 and beta-catenin We developed mouse genetic models that lack either Sox9, β-catenin, or both specifically in the somatic cells. All embryos used in this study resulted from the crossing between Ctnnb1f/f; Sox9f/f females with Sf1-cre+/Tg ; Ctnnb1+/f; Sox9+/f males. XX and XY fetal gonads were collected at embryonic day E14.5

2015-05-26 | E-GEOD-67463 | biostudies-arrayexpress

Purification and transcriptomic analysis of mouse fetal Leydig cells reveals candidate genes for disorders of sex development

Project description:To examine the transcriptome of early testicular somatic cells during gonadogenesis at 12.5dpc RNA sequencing (RNA-Seq) was performed on murine primary testicular cell lineages isolated from the Sf1-eGFP line by FACS. The three main somatic cell lineages of the testis were isolated: the Sertoli cells which direct male development; the fetal Leydig cells (FLCs) that produce steroid hormones and virilise the XY individual and a heterogenous population of interstitial cells, some of which give rise to the adult Leydig cells (ALCs). This dataset provides a platform for exploring the biology of FLCs and understanding the role of these cells in testicular development and masculinization of the embryo, and a basis for targeted studies designed to identify causes of idiopathic XY DSD. RNA-Seq of 3 enriched cell populations from 12.5dpc mouse gonad (Sertoli cells, Leydig cells and Interstitial cells isolated by FACS-sorting) on an Illumina HiSeq 1500, in triplicate.

2015-05-21 | E-GEOD-65498 | biostudies-arrayexpress

Jafarnejad2019 - Mechanistically detailed systems biology modeling of the HGF/Met pathway in hepatocellular carcinoma

Project description:Hepatocyte growth factor (HGF) signaling through its receptor Met has been implicated in hepatocellular carcinoma tumorigenesis and progression. Met interaction with integrins is shown to modulate the downstream signaling to Akt and ERK (extracellular-regulated kinase). In this study, we developed a mechanistically detailed systems biology model of HGF/Met signaling pathway that incorporated specific interactions with integrins to investigate the efficacy of integrin-binding peptide, AXT050, as monotherapy and in combination with other therapeutics targeting this pathway. Here we report that the modeled dynamics of the response to AXT050 revealed that receptor trafficking is sufficient to explain the effect of Met-integrin interactions on HGF signaling. Furthermore, the model predicted patient-specific synergy and antagonism of efficacy and potency for combination of AXT050 with sorafenib, cabozantinib, and rilotumumab. Overall, the model provides a valuable framework for studying the efficacy of drugs targeting receptor tyrosine kinase interaction with integrins, and identification of synergistic drug combinations for the patients. Model is encoded by Johannes and submitted to BioModels by Ahmad Zyoud.

2020-03-20 | MODEL2003200001 | BioModels

Dicer deficiency reveals microRNAs predicted to control gene expression in developing adrenal cortex [array]

Project description:MicroRNAs (miRNAs) are small, endogenous, non-protein coding RNAs that are an important means of post-transcriptional gene regulation. Deletion of Dicer, a key miRNA processing enzyme, is embryonic lethal in mice, and tissue-specific Dicer deletion results in developmental defects. Using a conditional knockout model, we generated mice lacking Dicer in the adrenal cortex. These Dicer knockout (KO) mice exhibited perinatal mortality and failure of the adrenal cortex during late gestation between embryonic day 16.5 (E16.5) and E18.5. Further study of Dicer KO adrenals demonstrated a significant loss of Sf1 expressing cortical cells that was histologically evident as early as E16.5 coincident with an increase in p21 and cleaved-caspase 3 staining in the cortex. However, peripheral cortical proliferation persisted in KO adrenals as assessed by anti-PCNA staining. To further characterize the embryonic adrenals from Dicer KO mice, we performed microarray analyses for both gene expression and miRNA on purified RNA isolated from control and KO adrenals of E15.5 and E16.5 embryos. Consistent with the absence of Dicer and the associated loss of miRNA-mediated mRNA degradation, we observed an up-regulation of a small subset of adrenal transcripts in Dicer KO mice, most notably the transcripts coded by the genes Nr6a1 and Acvr1c. Indeed, several miRNAs, including let-7, miR-34c, and miR-21 that are predicted to target these genes for degradation, were also markedly down-regulated in Dicer KO adrenals. Together these data suggest a role for miRNA mediated regulation of a subset of genes that are essential for normal adrenal growth and homeostasis. Adrenals from control and Dicer KO litter mates were pooled separately from 4 individual litters, resulting in a total of 4 control (cre-) and 4 Dicer KO biological replicates at both E15.5 and E16.5.

2013-05-01 | E-GEOD-45592 | biostudies-arrayexpress

Dicer deficiency reveals microRNAs predicted to control gene expression in developing adrenal cortex [RT-PCR]

2013-05-01 | E-GEOD-45810 | biostudies-arrayexpress

Gene expression profiling of SF1 in mouse uterus tissues

2016-04-14 | GSE66963 | GEO

RNA-seq Reveals Paxillin as a Key Facilitator of Endothelial Cell Migration and Angiogenesis after Spinal Cord Injury

Project description:Spinal cord injury (SCI) is a catastrophic condition resulting in significant neurological deficits. To map the altered pathways within the lesion epicenter and the surrounding rostro-caudal segments, we employed RNA-seq on injured spinal cord tissue. We sequenced samples from three level (rostral, epicenter, and caudal) at days 1, 14, and 28 post-injury to systematically define the transcriptomics profile, aiming to identify pathways related to angiogenesis after SCI. Gene set enrichment analysis (GSEA) revealed enriched pathways, including hepatocyte growth factor (HGF) receptor signalling and alpha-6 beta-4 signaling pathway, suggesting an active angiogenic signature. Furthermore, the participating genes in HGF receptor signaling were validated by qPCR analysis, demonstrating that HGF receptor signaling is involved in the pathological remodeling following SCI. Subsequently, we investigated paxillin as a candidate gene promoting endothelial cell migration through HGF receptor signaling. Immunohistochemistry data suggest paxillin’s role in mediating the endothelial cell migration and proliferation post-SCI. In summary, our findings indicate that paxillin is a key mediator of endothelial cell proliferation and migration in response to angiogenic factors like HGF following SCI. However, extensive mechanistic studies are required to fully establish paxillin’s role in endothelial cell migration and proliferation after SCI.

2025-05-20 | GSE277295 | GEO

Expression data of RPTEC cells treated with/without HGF, aMD5-PEG11 and aMD5-BMH

Project description:We synthesized HGF mimic Met-agonist, which is a kind of Met high-affinity dimeric peptide that can activate the Met through dimerization of Met, and induce cell growth, migration, and branching morphogenesis in a similar manner to HGF. Here we detected the gene expression profile induced by HGF and artificial Met-agonist (aMD5-PEG11 and aMD5-BMH). HGF and aMD5-PEG11 show similar induction of gene expression pattern, including multicellular organismal development, multicellular organismal process and anatomical structure development.

2018-11-30 | GSE111542 | GEO

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