Project description:Cisplatin (DDP) is a widely used chemotherapeutic agent that induces apoptosis in various cancer cells, but its effects on endothelial cells such as HMEC-1 (Human Microvascular Endothelial Cell line-1) are less well understood. This study aims to explore the transcriptional response of HMEC-1 to cisplatin treatment. RNA-seq analysis was performed to identify differentially expressed genes following cisplatin stimulation, providing insights into the molecular mechanisms underlying the cellular response to chemotherapy in endothelial cells. The results highlight key pathways and genes involved in the stress response, apoptosis, and cellular survival in HMEC-1 cells upon cisplatin treatment.
Project description:Cisplatin (DDP) is a widely used chemotherapeutic agent that induces apoptosis in various cancer cells, but its effects on endothelial cells such as HUVEC (Human Umbilical Vein Endothelial Cells) are less well understood. This study aims to explore the transcriptional response of HUVEC cells to cisplatin treatment. RNA-seq analysis was performed to identify differentially expressed genes following cisplatin stimulation, providing insights into the molecular mechanisms underlying the cellular response to chemotherapy in endothelial cells. The results highlight key pathways and genes involved in the stress response, apoptosis, and cellular survival in HUVEC cells upon cisplatin treatment.
Project description:Analysis of gene expression in immortalized human microvascular endothelial cells (TIME cells) following forced expression of the JunB. Results provide insight into a role for the JunB signaling pathway in endothelial cell.
Project description:Heparan sulfate (HS) in the vascular endothelial glycocalyx (eGC) is a critical regulator of blood vessel homeostasis. Trauma results in HS shedding from the eGC, but the impact of HS shedding on mechanisms of vascular injury and repair has not been evaluated. The objective of this work was to characterize the effect of eGC HS shedding on the transcriptional landscape of vascular endothelial cells. In vitro work was performed using flow conditioned primary human lung microvascular ECs treated with vehicle or heparin lyase III to simulate human heparanase activity. Bulk RNA sequencing was performed to determine differentially expressed gene-enriched pathways following heparin lyase III treatment. Pathway analysis demonstrated downregulation of genes that support cell junction integrity, EC polarity, and EC senescence while upregulating genes that promote cell differentiation and proliferation following HS shedding.