ARPCs Can Revert Lps-Induced Endothelial-to-Mesenchymal Transition of Endothelial Cells
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ABSTRACT:
PROVIDER: PRJNA480439 | ENA |
REPOSITORIES: ENA
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Project description:Endothelial dysfunction is a hallmark of LPS-induced acute kidney injury (AKI). Endothelial cells (EC) acquired a fibroblast-like phenotype and contributed to myofibroblasts generation through Endothelial to Mesenchymal Transition (EndMT) process. Noteworthy, ARPCs enhance tubular regenerative mechanism during AKI, but little is known about their effects on EC. Here we investigated whether ARPCs could prevent sepsis-induced EndMT and the related mechanism. When activated by LPS, Human endothelial cells (EC) proliferated and decreased specific EC markers such as CD31 and VE-cadherin and up-regulated myofibroblast markers such as Collagen I and Vimentin. The co-culture with ARPCs normalized EC proliferation rate and abrogated the LPS-induced EndMT by restoring the high expression of EC markers and the low expression of myofibroblast markers. Gene set enrichment analysis showed that most of genes modulated in LPS-stimulated ARPCs belongs to cell activation and defense response pathways. In particular, among most up-regulated genes we found BPIFA2, SAA2, SAA4 and CXCL6. BPIFA2 is recently described as an early biomarker of AKI but little is known about its function in the kidney. The other genes are frequently involved in the response to bacterial infection and kidney injury. Finally, in a swine model of LPS-induced AKI, we observed an increase of CD133+ARPCs that expressed BPIFA2 respect to healthy pigs. Taken together, these results suggest an underestimate role of ARPCS in preventing endothelial dysfuncton by the production of several proteins. The identification of these molecules may offer novel strategies to protect endothelial compartment and promote kidney repair.
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Project description:This SuperSeries is composed of the following subset Series: GSE15933: Analysis of Gene Expression changes in human intestinal endothelial-to-mesenchymal transition - UNTREATED/CONTROL GROUP GSE15934: Analysis of Gene Expression changes in human intestinal endothelial-to-mesenchymal transition - TRANSFORMED GROUP Refer to individual Series
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Project description:To investigate the transcriptome of endothelial cells undergoing endothelial-to-mesenchymal transition, transcription profiling was performed on primary human endothelial cells in the presence or absence of 40mM acetate following control or cytokine treatment for 4 days. We then performed gene expression profiling analysis using data obtained from RNA-seq of primary human endothelial cells.
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Project description:The histone demethylase JMJD2B regulates endothelial-to-mesenchymal transition
| PRJNA599370 | ENA
Project description:Endothelial-mesenchymal transition (EndMT) is a complex process, in which differentiated endothelial cells undergo phenotypic transition to mesenchymal cells. Given the diversity of the vascular system in architecture, structure, and embryonic origins, it is not clear if endothelial cells lining different vessels are able to undergo EndMT. Therefore, the aim of this study was to evaluate the molecular and functional changes that occur in different types of endothelial cells after induction of EndMT through overexpression of Snail and TGF-β2. Different types of endothelial cells (human umbilical vein, heart, and lung) have distinct response when induced to undergo EndMT. Coronary artery endothelial cells (HCAEC) induced with combined Snail overexpression plus TGF-β2 treatment promotes a decrease of endothelial markers, an increase of mesenchymal markers and migration. The mechanism that HCAEC undergoing EndMT may be mediated through Notch and non-canonical Wnt signaling pathways. These results provide the foundation for understanding the roles of specific signaling pathways in mediating EndMT in endothelial cells from different anatomical origin.
2017-04-22 | GSE96089 | GEO
Project description:Endothelial cells play an important role in maintenance of the vascular system and the repair after injury. Under pro-inflammatory conditions, endothelial cells can acquire a mesenchymal phenotype by a process named endothelial-to-mesenchymal transition (EndMT), which affects the functional properties of endothelial cells. Here, we investigated the epigenetic control of EndMT. We show that the histone demethylase JMJD2B is induced by EndMT promoting pro-inflammatory and hypoxic conditions. Silencing of JMJD2B reduced TGF-β2-induced expression of mesenchymal genes and prevented the alterations in endothelial morphology and impaired endothelial barrier function. Endothelial-specific deletion of JMJD2B in vivo confirmed a reduction of EndMT after myocardial infarction. EndMT did not affect global H3K9me3 levels but induced a site-specific reduction of repressive H3K9me3 marks at promoters of mesenchymal genes, such as Calponin (CNN1), and genes involved in TGF-β signaling, such as AKT Serine/Threonine Kinase 3 (AKT3) and sulfatase 1 (SULF1). Silencing of JMJD2B prevented the EndMT-induced reduction of H3K9me3 marks at these promotors and further repressed these EndMT-related genes. Our study reveals that endothelial identity and function is critically controlled by the histone demethylase JMJD2B, which is induced by EndMT-promoting pro-inflammatory and hypoxic conditions and support the acquirement of a mesenchymal phenotype.
2020-01-08 | GSE143150 | GEO
Project description:Endothelial cells play an important role in maintenance of the vascular system and the repair after injury. Under pro-inflammatory conditions, endothelial cells can acquire a mesenchymal phenotype by a process named endothelial-to-mesenchymal transition (EndMT), which affects the functional properties of endothelial cells. Here, we investigated the epigenetic control of EndMT. We show that the histone demethylase JMJD2B is induced by EndMT promoting pro-inflammatory and hypoxic conditions. Silencing of JMJD2B reduced TGF-β2-induced expression of mesenchymal genes and prevented the alterations in endothelial morphology and impaired endothelial barrier function. Endothelial-specific deletion of JMJD2B in vivo confirmed a reduction of EndMT after myocardial infarction. EndMT did not affect global H3K9me3 levels but induced a site-specific reduction of repressive H3K9me3 marks at promoters of mesenchymal genes, such as Calponin (CNN1), and genes involved in TGF-β signaling, such as AKT Serine/Threonine Kinase 3 (AKT3) and sulfatase 1 (SULF1). Silencing of JMJD2B prevented the EndMT-induced reduction of H3K9me3 marks at these promotors and further repressed these EndMT-related genes. Our study reveals that endothelial identity and function is critically controlled by the histone demethylase JMJD2B, which is induced by EndMT-promoting pro-inflammatory and hypoxic conditions and support the acquirement of a mesenchymal phenotype.
2020-01-08 | GSE143148 | GEO