Project description:Eltd1 is widely expressed in endothelial cells. We have reported that the expression of Eltd1 is highly up-regulated in glioma vessels. Other studies have shown that Eltd1 is up-regulated in vessels in other types of tumors, and has been suggested as a vascular target for anti-angiogenesis therapy. However, the role of Eltd1 in vessels is largely unknown. We isolated endothelial cells from healthy brain tissue and GL261 tumor tissue, and analyzed the role of Eltd1 in tumor angiogenesis by analyzing the endothelial gene profile from wild type and Eltd1-/- mice.
Project description:The purpose is to obtain samples for microRNA analysis in primary human microvascular endothelial cells infected with wild type MERS-CoV (icMERS).
Project description:The purpose is to obtain samples for mRNA analysis in primary human microvascular endothelial cells infected with wild type MERS-coronavirus (MERS-CoV) (icMERS).
Project description:Single cell RNAseq from brain endothelial cells (BECs) isolated from wild-type and Iqgap2-/- (KO) mice to identify transcriptional changes in BECs caused by loss of Iqgap2. Mouse brains were dissociated to single cell suspension and labelled with CD31. CD31+ cells were flow sorted and processed for single cell RNAseq.
Project description:The purpose is to obtain samples for mRNA analysis in primary human microvascular endothelial cells infected with wild type MERS-CoV (icMERS).
Project description:Gene expression profile at single cell level of muscle endothelial cells (ECs) and muscle non-ECs from wild type and tumor bearing mice
Project description:Loss of Pten in the KrasG12D;Amhr2-Cre mutant mice leads to the transformation of ovarian surface epithelial (OSE) cells and rapid development of low-grade, invasive serous adenocarcinomas. Tumors occur with 100% penetrance and express elevated expression of wild type tumor repressor protein 53 (TRP53). To test the functions of TRP53 in the Pten;Kras (Trp53+) mice, we disrupted the Trp53 gene yielding Pten;Kras(Trp53-) mice. By comparing morphology and gene expression profiles in the Trp53+ and Trp53- OSE cells, we document that wild-type TRP53 acts as a major promoter of OSE cell survival and differentiation: cells lacking Trp53 are transformed yet are less adherent, migratory and invasive and exhibit a gene expression profile more like normal OSE cells. These results provide a new paradigm: wild type TRP53 does not preferentially induce apoptotic or senescent related genes in the Pten;Kras(Trp53+) cancer cells but rather increases genes regulating DNA repair, cell cycle progression and proliferation and decreases putative tumor suppressor genes. However, if TRP53 activity is forced higher by exposure to nutlin-3a (an MDM2 antagonist), TRP53 suppresses DNA repair genes and induces the expression of genes that control cell cycle arrest and apoptosis. Thus, in the Pten;Kras(Trp53+) mutant mouse OSE cells and likely in human TP53+ low grade ovarian cancer cells, wild type TRP53 controls global molecular changes that are dependent on its activation status. These results suggest that activation of TP53 may provide a promising new therapy for managing type I ovarian cancer and other cancers in humans where wild-type TP53 is expressed.