Identification of endothelial derived factors that promote metastasis I
Ontology highlight
ABSTRACT: To identify endothelial-derived factors that may instructively drive cancer metastasis, we generated a new mouse model that allows endothelial-specific ribosomal tagging. We crossed the RiboTag (Rpl22fl/flHA) mice with the endothelial inducible Cre line Cdh5(PAC)-CreERT2 mice. Endothelial derived ribosome-associated mRNA-sequencing was performed from highly metastatic B16F10 and poorly metastatic B16F0 tumours.
Project description:To identify endothelial-derived factors that may instructively drive cancer metastasis, we generated a new mouse model that allows endothelial-specific ribosomal tagging. We crossed the RiboTag (Rpl22fl/flHA) mice with the endothelial inducible Cre line Cdh5(PAC)-CreERT2 mice. Endothelial derived ribosome-associated mRNA-sequencing was performed from highly metastatic B16F10 and poorly metastatic B16F0 tumours.
Project description:To identify endothelial-derived factors that may instructively drive cancer metastasis, we generated a new mouse model that allows endothelial-specific ribosomal tagging. We crossed the RiboTag (Rpl22fl/flHA) mice with the endothelial inducible Cre line Cdh5(PAC)-CreERT2 mice. Endothelial derived ribosome-associated mRNA-sequencing was performed from highly metastatic B16F10 and poorly metastatic B16F0 tumours.
Project description:We report the gene expression profiles of control IgG and anti-Dll4 Ab treated retinal endothelial cells (ECs) in EC-specific RiboTag mouse (Cdh5-CreERT2 Rpl22 tm1.1Psam )
Project description:Gata4 is required for mouse endocardium development. To identify genes regulated by Gata4 in endocardium, we deleted Gata4 in endocardium with Cdh5(Pac)-CreERT2 and performed single cell RNA sequencing (scRNA-seq) to analyze all cells from the ventricles.
Project description:Under the hypothesis that subset of parental cells may already harbor metastasis potential, which leads progression of metastasis, we investigated single-cell expression of parental B16 melanoma cell (B16F0) and its highly metastatic subclone (B16F10) (N=4,156) using single-cell RNA sequencing
Project description:To study the effects of the loss of Sox7 function on gene expression of the endothelium in vivo during development. We generated a endothelial specific ko using a Sox7fl/fl Cdh5 creERT2 inducible system.
Project description:To study the effects of the loss of Sox7 function on gene expression of the endothelium in vivo during development. We generated a endothelial specific ko using a Sox7fl/fl Cdh5 creERT2 inducible system.
Project description:To identify potential biological targets of the TGFβ pathway involved in AVM formation, we performed RNA-seq on endothelial cells (ECs) isolated from a Smad4 inducible, EC specific knockout (Smad4-iECKO; Smad4f/f;Cdh5-CreERT2) mouse model that develops retinal AVMs.
Project description:To identify tumor-specific transcriptional changes following SX-682 treatment, we performed RNA sequencing on each of the MelanA, B16F0, and B16F10 cell lines.
Project description:Uncontrolled accumulation of pulmonary artery smooth muscle cells (PASMC) to the distal pulmonary arterioles (PAs) is one of the major characteristics of pulmonary hypertension (PH). Cellular senescence contributes to aging and lung diseases associated with PH and links to PH progression. However, the mechanism by which cellular senescence controls vascular remodeling in PH is not fully understood. The levels of senescence marker, p16INK4A and senescence-associated β-galactosidase (SA-β-gal) activity are higher in PA endothelial cells (ECs) isolated from idiopathic pulmonary arterial hypertension (IPAH) patients compared to those from healthy individuals. Hypoxia-induced accumulation of α-smooth muscle actin (αSMA)-positive cells to the PAs is attenuated in p16fl/fl-Cdh5(PAC)-CreERT2 (p16iΔEC) mice after tamoxifen induction. We have reported that endothelial TWIST1 mediates hypoxia-induced vascular remodeling by increasing platelet-derived growth factor (PDGFB) expression. Transcriptomic analyses of IPAH patient or hypoxia-induced mouse lung ECs reveal the alteration of senescence-related gene expression and their interaction with TWIST1. Knockdown of p16INK4A attenuates the expression of PDGFB and TWIST1 in IPAH patient PAECs or hypoxia-treated mouse lungs and suppresses accumulation of αSMA–positive cells to the supplemented ECs in the gel implanted on the mouse lungs. Hypoxia-treated mouse lung EC-derived exosomes stimulate DNA synthesis and migration of PASMCs in vitro and in the gel implanted on the mouse lungs, while p16iΔEC mouse lung EC-derived exosomes inhibit the effects. These results suggest that endothelial senescence controls αSMA–positive cell proliferation and migration in PH through TWIST1-PDGFB signaling.