Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA340983 | ENA |
REPOSITORIES: ENA
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Project description:Analysis of ex vivo isolated lymphatic endothelial cells from the dermis of patients to define type 2 diabetes-induced changes. Results preveal aberrant dermal lymphangiogenesis and provide insight into its role in the pathogenesis of persistent skin inflammation in type 2 diabetes. The ex vivo dLEC transcriptome reveals a dramatic influence of the T2D environment on multiple molecular and cellular processes, mirroring the phenotypic changes seen in T2D affected skin. The positively and negatively correlated dLEC transcripts directly cohere to prolonged inflammatory periods and reduced infectious resistance of patients´ skin. Further, lymphatic vessels might be involved in tissue remodeling processes during T2D induced skin alterations associated with impaired wound healing and altered dermal architecture. Hence, dermal lymphatic vessels might be directly associated with T2D disease promotion. Global gene expression profile of normal dermal lymphatic endothelial cells (ndLECs) compared to dermal lymphatic endothelial cells derived from type 2 diabetic patients (dLECs).Quadruplicate biological samples were analyzed from human lymphatic endothelial cells (4 x diabetic; 4 x non-diabetic). subsets: 1 disease state set (dLECs), 1 control set (ndLECs)
2012-06-01 | E-GEOD-38396 | biostudies-arrayexpress
Project description:Diabetes is prevalent worldwide and associated with severe health complications, including blood vessel damage that leads to cardiovascular disease and death. We report the development of 3D blood vessel organoids from human embryonic and induced pluripotent stem cells. These human blood vessel organoids contain endothelium, perivascular pericytes, and basal membranes, and self-assemble into lumenized interconnected capillary networks. We treat these vascular organoids with hyperglycemia and inflammatory cytokines in vitro, which leads to basement membrane thickening, a structural hallmark of diabetic patient. To compare differential gene expression we performed RNAseq on endothelial cells, derived from control (NG) or diabetic (DI) vascular organoids.
2018-08-01 | GSE89475 | GEO
Project description:Transcriptomic Analysis of Endothelial Cells from Fibrovascular Membranes in Proliferative Diabetic Retinopathy
| PRJNA363068 | ENA
Project description:Vascular endothelial cells play a pivotal role in whole body homeostasis. Recent advances have revealed enhancer-associated long non-coding RNAs as essential regulators in endothelial function. We investigated LINC00607, a super enhancer-derived in human arteries with an emphasis on endothelial cells. Using a series of RNA-sequencing, we characterized the transcriptomes regulated by LINC00607 in endothelial cells and vascular smooth muscle cells, and in basal and diabetic conditions in endothelial cells. Furthermore, using scRNA-seq, we demonstrated that modified antisense oligonucleotide inhibitor of LINC00607 can reverse key dysfunctional changes induced by high glucose and TNF-alpha in endothelial cells.
2022-07-20 | GSE197955 | GEO
Project description:Vascular endothelial cells play a pivotal role in whole body homeostasis. Recent advances have revealed enhancer-associated long non-coding RNAs as essential regulators in endothelial function. We investigated LINC00607, a super enhancer-derived in human arteries with an emphasis on endothelial cells. Using a series of RNA-sequencing, we characterized the transcriptomes regulated by LINC00607 in endothelial cells and vascular smooth muscle cells, and in basal and diabetic conditions in endothelial cells. Furthermore, using scRNA-seq, we demonstrated that modified antisense oligonucleotide inhibitor of LINC00607 can reverse key dysfunctional changes induced by high glucose and TNF-alpha in endothelial cells.
2022-07-20 | GSE197954 | GEO
Project description:Endothelial cells derived from iPSC in response to diabetic medium
| PRJNA352279 | ENA
Project description:Diabetes is a known risk factor for various cardiovascular complications, mediated by endothelial dysfunction. Despite the high prevalence of this metabolic disorder, there is a lack of in vitro models that recapitulate the complexity of genetic and environmental factors associated with diabetic endothelial dysfunction. Here, we utilized human induced pluripotent stem cell (iPSC)-derived endothelial cells (ECs) to develop in vitro models of diabetic endothelial dysfunction. We found that the diabetic phenotype was recapitulated in diabetic patient-derived iPSC-ECs, even in the absence of a diabetogenic environment. Subsequent exposure with culture conditions that mimic the diabetic clinical chemistry induced a diabetic phenotype in healthy iPSC-ECs but did not affect the already dysfunctional diabetic iPSC-ECs. RNA-seq analysis revealed extensive transcriptome-wide differences between cells derived from healthy individuals and diabetic patients. The in vitro disease models were used as a screening platform which identified angiotensin receptor blockers (ARBs) that improved endothelial function in vitro for each patient. In summary, we present in vitro models of diabetic endothelial dysfunction using iPSC technology, taking into account the complexity of genetic and environmental factors in the metabolic disorder. Our study provides novel insights into the pathophysiology of diabetic endothelial dysfunction and highlights the potential of iPSC-based models for drug discovery and personalized medicine.
2023-07-05 | GSE236430 | GEO
Project description:Reference epigenomes of human vascular endothelial cells
| PRJNA532996 | ENA