Endothelial to Mesenchymal Transition
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE56309 | GEO | 2016/04/05
SECONDARY ACCESSION(S): PRJNA242886
REPOSITORIES: GEO
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Project description:Driving HUVECs toward mesenchymal fate Comparison of untreated HUVECs, HUVECs treated with TGF-B, HUVECS treated with TGF-B and oxidative stress, and comparator human dermal fibroblasts
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Project description:The tumor microenvironment (TME) of non-small cell lung cancer (NSCLC) is highly heterogeneous and is involved in tumorigenesis and resistance to therapy. Among the cells of the TME, endothelial cells are associated with the latter processes through endothelial-to-mesenchymal transition (EndMT). During EndMT, endothelial cells (ECs) progressively lose their endothelial phenotype in favor of a mesenchymal phenotype, which favors the production of cancer-associated fibroblasts. Our study aimed to investigate the consequences of exposure to different lung tumor secretomes on EC phenotype and plasticity. Conditioned media (CM) were prepared from the tumor cell lines A549, H1755, H23, H1437 and H1975. Proliferation and migration of endothelial cells treated with these CMs were assessed by Cyquant® and Incucyte® technologies, respectively. The angiogenic capacity of ECs was assessed by following tubulogenesis on Matrigel®. Phenotypic changes in treated ECs were detected by flow cytometry. Morphological analysis of actin fibers was performed by immunohistochemistry, while proteomic analysis by mass spectrometry was used to identify the protein content of secretomes. A change of the endothelial phenotype was found when HUVECs were treated with different CMs. This phenotypic change was associated with a morphological change, an increase in both stress fiber expression and spontaneous migration. Furthermore, an increase in mesenchymal markers (±-SMA and CD44) confirmed the phenotypic changes. However, the secretomes did not modify the rate of double-labelled cells (vWF+/-SMA+ or CD31+/CD44+). Proteomic analysis identified potential targets involved in the EndMT with therapeutic relevance. Taken together, these data suggest that CMs are capable of inducing partial EndMT.
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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.
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