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The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [single-cell RNA-seq]

ABSTRACT: Microarray, Bulk RNA Sequencing and Single cell RNA Sequencing of different murine tissue-resident macrophage populations to assess role of Zeb2 and LXRa

ORGANISM(S): Mus musculus

PROVIDER: GSE117079 | GEO | 2018/07/14

REPOSITORIES: GEO

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The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [microarray]

Project description:Microarray, Bulk RNA Sequencing and Single cell RNA Sequencing of different murine tissue-resident macrophage populations to assess role of Zeb2 and LXRa

2018-07-14 | GSE117080 | GEO

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [bulk RNA-seq]

Project description:Microarray, Bulk RNA Sequencing and Single cell RNA Sequencing of different murine tissue-resident macrophage populations to assess role of Zeb2 and LXRa

2018-07-14 | GSE117078 | GEO

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages

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

2018-07-14 | GSE117081 | GEO

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [bulk RNA-seq]

Project description:The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [bulk RNA-seq]

| PRJNA481019 | ENA

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages

Project description:The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages

| PRJNA481016 | ENA

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [microarray]

Project description:The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [microarray]

| PRJNA481018 | ENA

The Transcription Factor ZEB2 Is Required to Maintain the Tissue-Specific Identities of Macrophages.

Project description:Heterogeneity between different macrophage populations has become a defining feature of this lineage. However, the conserved factors defining macrophages remain largely unknown. The transcription factor ZEB2 is best described for its role in epithelial to mesenchymal transition; however, its role within the immune system is only now being elucidated. We show here that Zeb2 expression is a conserved feature of macrophages. Using Clec4f-cre, Itgax-cre, and Fcgr1-cre mice to target five different macrophage populations, we found that loss of ZEB2 resulted in macrophage disappearance from the tissues, coupled with their subsequent replenishment from bone-marrow precursors in open niches. Mechanistically, we found that ZEB2 functioned to maintain the tissue-specific identities of macrophages. In Kupffer cells, ZEB2 achieved this by regulating expression of the transcription factor LXRα, removal of which recapitulated the loss of Kupffer cell identity and disappearance. Thus, ZEB2 expression is required in macrophages to preserve their tissue-specific identities.

| S-EPMC6104815 | biostudies-literature

The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [single-cell RNA-seq]

Project description:The Transcription factor Zeb2 ia required to maintain tissue-specific identities of macrophages [single-cell RNA-seq]

| PRJNA481017 | ENA

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.

2021-03-23 | PXD022212 | Pride

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)

2016-03-15 | E-GEOD-27966 | biostudies-arrayexpress

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