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The role of endothelial Zeb2 in the progression of non-alcoholic fatty liver disease

ABSTRACT: Zinc-Finger E-Box-binding Homeobox (Zeb)2 has an anti-angiogenic and anti-fibrotic role in liver endothelial cells, but its role in non-alcoholic fatty liver disease remains unknown. We performed RNA sequencing on endothelial cells sorted from wild-type mice and mice lacking Zeb2 specifically in endothelial cells kept on a western or standard diet to identify RNA expression changes and gene ontology terms affected by knock-out of endothelial Zeb2, western diet challenge, or the combination of both challenges.

ORGANISM(S): Mus musculus

PROVIDER: GSE224595 | GEO | 2025/07/02

REPOSITORIES: GEO

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Endothelial loss of Zeb2 distorts the hepatic angioarchitecture and aggravates liver fibrosis in mice

Project description:Expression of the Zinc-Finger E-Box-binding Homeobox (Zeb)2 is enriched in Liver Sinusoidal Endothelial cells (LSECs), but its role in liver ECs remains unknown. We performed RNA sequencing on the main liver cell types from wild-type mice and mice lacking Zeb2 specifically in endothelial cells to identify cell-autonomous and non-autonomous RNA expression changes and to find pathways and GO-terms affected by genetic Zeb2 inactivation.

2022-03-30 | GSE150699 | GEO

Identification of ZEB2 binding sites in Hepatocellular Carcinoma Cell Line SNU398

Project description:ZEB2, a member of the ZEB family of EMT inducers, is involved in cellular proliferation, senescence, and invasion in most of the human cancers. However, genes regulated by ZEB2 in hepatocellular carcinoma (HCC) are not identified so far. Hence, we conducted a ChIP-Seq study in high ZEB2 expressing HCC cell line SNU398 by using a homemade anti-ZEB2 antibody (clone 6E5).

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ZEB2 protects the heart from ischemic damage

Project description:infarct size and subsequent deterioration in function. The identification of factors that enhance cardiac repair by the restoration of the vascular network is, therefore, of great significance. Here, we show that the transcription factor Zinc finger E-box-binding homeobox 2 (ZEB2) is increased in stressed cardiomyocytes and induces a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia. Single-cell sequencing indicates ZEB2 to be enriched in injured cardiomyocytes. Cardiomyocyte-specific deletion of ZEB2 results in impaired cardiac contractility and infarct healing post-myocardial infarction (post-MI), while cardiomyocyte-specific ZEB2 overexpression improves cardiomyocyte survival and cardiac function. We identified Thymosin 4 (TMSB4) and Prothymosin (PTMA) as main paracrine factors released from cardiomyocytes to stimulate angiogenesis by enhancing endothelial cell migration, and whose regulation is validated in our in vivo models. Therapeutic delivery of ZEB2 to cardiomyocytes in the infarcted heart induces the expression of TMSB4 and PTMA, which enhances angiogenesis and prevents cardiac dysfunction. These findings reveal ZEB2 as a beneficial factor during ischemic injury, which may hold promise for the identification of new therapies.

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The role of endothelial Zeb2 in the progression of non-alcoholic fatty liver disease

Project description:The role of endothelial Zeb2 in the progression of non-alcoholic fatty liver disease

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Loss of ZEB2 in basal breast cancer cells

Project description:Study of loss of ZEB2 in breast cancer cells in vitro and in vivo: gene expression and phenotypic switch to more benign behavior of the cancer cells. Morphological, functional and gene microarray analysis following ZEB2 knockdown in MDAMB231 cells reveals gain of epithelial differentiation, reduction of migration, invasion and metastatic capability. The measurement of ZEB2 transcriptional activity in tumor cells efficiently predicts the probability of breast cancer patient survival. Global gene expression profiles were measured using Affymetrix U133 plus2 microarrays in MDAMB231 cells (control and ZEB2 shRNA and siRNA knockdown cells on plastic)

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ZEB2 locus regulation in differentiating iPSCs

Project description:The multi-domain transcription factor ZEB2 controls embryonic and adult cell fate decisions and maturation in many stem/progenitor cell types. Defects in these processes in specific cell types underlie Mowat-Wilson syndrome (MOWS), which is caused by ZEB2 haplo-insufficiency. Human ZEB2, like mouse Zeb2, is located on chromosome 2 downstream of an approximately 3.5 Mb-long gene-desert, lacking any protein-coding gene sequence. Using temporal high-resolution Targeted Chromatin Capture (T2C), we show major chromatin structural changes based on mapping in-cis proximities between the ZEB2 gene promoter and this gene desert during neural differentiation of induced pluripotent cells (iPSCs), including at early neuroprogenitor cell (NPC)/rosette state, where ZEB2 mRNA levels increase significantly. Combining T2C with histone-3 acetylation mapping, we identified three novel candidate enhancers about 500 kb upstream of the ZEB2 transcription start site (TSS). Functional luciferase-based assays in heterologous cells and NPCs reveal co-operation between these three enhancers. This study is the first to document in-cis regulatory elements (REs) located in ZEB2’s gene desert. The results further show the usability of T2C for future studies of ZEB2 REs in differentiation and maturation of relevant cell types, and the molecular characterization of identified MOWS patients that lack mutations in ZEB2 protein-coding exons.

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The transcription factors ZEB2 and T-bet cooperate to program cytotoxic T cell terminal differentiation

Project description:T-bet is critical for cytotoxic T lymphocyte (CTL) differentiation, but it is unclear how it operates in a graded manner in the formation of both terminal effector and memory precursor cells during infection. We find that at high concentrations T-bet induced expression of Zeb2 mRNA, which then triggered CTLs to adopt terminally differentiated states. ZEB2 and T-bet cooperate to switch on a terminal CTL differentiation program, while simultaneously repressing genes necessary for central memory CTL development. Chromatin immunoprecipitation sequencing (ChIP-seq) showed that a large proportion of these genes were bound by T-bet, and this binding was altered by ZEB2 deficiency. Furthermore, T-bet overexpression could not fully bypass ZEB2 function. Thus, the coordinated actions of T-bet and ZEB2 outline a novel genetic pathway that forces commitment of CTLs to terminal differentiation, thereby restricting their memory cell potential. Splenocyte derived CD8+ T cells from C57BL/6 mice with either a wildtype (WT) (GzmB-Cre Zeb2+/+) or GzmB-Cre Zeb2-fl/fl (Zeb2-/-) backgrounds, following 8 days post infection with LCMV-Armstrong, were subsetted into KLRG1-hi/IL-7R-lo populations (terminal effectors, TE) or KLRG1-lo/IL-7R-hi (memory precursors, MP) populations. Four experimental groups, each with 3 samples, comprised of TE+WT, MP+WT, TE+ZEB2-/-, and MP+ZEB2-/-, were profiled for gene expression utilizing a polyA RNA prep and hybridized to the Illumina microarray platform IlluminaWG-v2.0.

2015-09-15 | E-GEOD-72408 | biostudies-arrayexpress

The regulatory role of ZEB2 in ABC formation

Project description:To elucidate the direct targets of ZEB2 in ABCs, we performed high-throughput sequencing of regulome by ATAC-seq, CUT & Tag, and CUT & RUN, leading to the identification the accessible sites with ZEB2 binding. Among the genes differentially expressed by Zeb2 deficiency, we found 33 candidate target genes of ZEB2, with 22 repressed and 11 activated by ZEB2. The critical transcription factor Mef2b, essential for GC development, was repressed by ZEB2. This direct regulation was mapped to a conserved region about 20kb downstream of Mef2b's exon I TSS, enriched with enhancer-associated features in both human and mouse.

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Expression data from WT cDC1s, Zeb2 KO cDC1s, Nfil3 Zeb2 DKO cDC1s and Zeb2 Id2 DKO cDC1s

Project description:Expression data from WT cDC1s, Zeb2 KO cDC1s, Nfil3 Zeb2 DKO cDC1s and Zeb2 Id2 DKO cDC1s

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ZEB2 is a Master Switch Controlling the Tumor-Associated Macrophage Program [KO_screen]

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