scholarly journals Inflammation induced insulin resistance is associated with DNA methylation changes in vascular endothelial cells

2017 ◽  
Vol 1 (Special Issue) ◽  
pp. 104-104 ◽  
Author(s):  
Aswath Balakrishnan ◽  
Kapaettu Satyamoorthy ◽  
Manjunath B. Joshi
Keyword(s):  
Insulin Resistance ◽  
Dna Methylation ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

scholarly journals Insulin resistance in vascular endothelial cells promotes intestinal tumour formation

Oncogene ◽  
2017 ◽  
Vol 36 (35) ◽  
pp. 4987-4996 ◽  
Author(s):  
X Wang ◽  
M-F Häring ◽  
T Rathjen ◽  
S M Lockhart ◽  
D Sørensen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Tumour Formation ◽  
Intestinal Tumour

scholarly journals Protein Arginine Methylation Is More Prone to Inhibition by S-Adenosylhomocysteine than DNA Methylation in Vascular Endothelial Cells

PLoS ONE ◽  
2013 ◽  
Vol 8 (2) ◽  
pp. e55483 ◽  
Author(s):  
Ruben Esse ◽  
Monica S. Rocha ◽  
Madalena Barroso ◽  
Cristina Florindo ◽  
Tom Teerlink ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Arginine Methylation ◽  
Vascular Endothelial ◽  
Protein Arginine Methylation

scholarly journals Epigenetic regulation of the lineage specificity of primary human dermal lymphatic and blood vascular endothelial cells

Angiogenesis ◽  
2020 ◽  
Author(s):  
Carlotta Tacconi ◽  
Yuliang He ◽  
Luca Ducoli ◽  
Michael Detmar
Keyword(s):  
Dna Methylation ◽  
Endothelial Cells ◽  
Molecular Mechanisms ◽  
Vascular Endothelial Cells ◽  
Transcriptional Level ◽  
Vascular Endothelial ◽  
Lineage Specificity ◽  
Endothelial Lineage ◽  
Lineage Markers ◽  
Developmental Features

Abstract Lymphatic and blood vascular endothelial cells (ECs) share several molecular and developmental features. However, these two cell types possess distinct phenotypic signatures, reflecting their different biological functions. Despite significant advances in elucidating how the specification of lymphatic and blood vascular ECs is regulated at the transcriptional level during development, the key molecular mechanisms governing their lineage identity under physiological or pathological conditions remain poorly understood. To explore the epigenomic signatures in the maintenance of EC lineage specificity, we compared the transcriptomic landscapes, histone composition (H3K4me3 and H3K27me3) and DNA methylomes of cultured matched human primary dermal lymphatic and blood vascular ECs. Our findings reveal that blood vascular lineage genes manifest a more ‘repressed’ histone composition in lymphatic ECs, whereas DNA methylation at promoters is less linked to the differential transcriptomes of lymphatic versus blood vascular ECs. Meta-analyses identified two transcriptional regulators, BCL6 and MEF2C, which potentially govern endothelial lineage specificity. Notably, the blood vascular endothelial lineage markers CD34, ESAM and FLT1 and the lymphatic endothelial lineage markers PROX1, PDPN and FLT4 exhibited highly differential epigenetic profiles and responded in distinct manners to epigenetic drug treatments. The perturbation of histone and DNA methylation selectively promoted the expression of blood vascular endothelial markers in lymphatic endothelial cells, but not vice versa. Overall, our study reveals that the fine regulation of lymphatic and blood vascular endothelial transcriptomes is maintained via several epigenetic mechanisms, which are crucial to the maintenance of endothelial cell identity.

The Endothelial Cell and the Factor VIII Bypassing Activity of Prothrombin Complex Concentrate

1988 ◽  
Vol 60 (02) ◽  
pp. 226-229 ◽  
Author(s):  
Jerome M Teitel ◽  
Hong-Yu Ni ◽  
John J Freedman ◽  
M Bernadette Garvey
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Factor Viii ◽  
Prothrombin Complex Concentrate ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Monolayer Cultures ◽  
Coagulant Activity ◽  
Time Courses ◽  
Privileged Site

SummarySome classical hemophiliacs have a paradoxical hemostatic response to prothrombin complex concentrate (PCC). We hypothesized that vascular endothelial cells (EC) may contribute to this “factor VIII bypassing activity”. When PCC were incubated with suspensions or monolayer cultures of EC, they acquired the ability to partially bypass the defect of factor VIII deficient plasma. This factor VIII bypassing activity distributed with EC and not with the supernatant PCC, and was not a general property of intravascular cells. The effect of PCC was even more dramatic on fixed EC monolayers, which became procoagulant after incubation with PCC. The time courses of association and dissociation of the PCC-derived factor VIII bypassing activity of fixed and viable EC monolayers were both rapid. We conclude that EC may provide a privileged site for sequestration of constituents of PCC which express coagulant activity and which bypass the abnormality of factor VIII deficient plasma.

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