Endothelin B Receptors on Vascular Smooth Muscle Cells of the Human Umbilical Vein Mediate Vasoconstriction

2008 ◽  
Vol 24 (1) ◽  
pp. 67-70 ◽  
Author(s):  
Eva Mildenberger ◽  
Beatrix Biesel ◽  
Günter Siegel ◽  
Hans T. Versmold
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Umbilical Vein ◽  
Muscle Cells ◽  
Human Umbilical Vein ◽  
Endothelin B

Stretch‐induced endothelin B receptor‐mediated apoptosis in vascular smooth muscle cells

2000 ◽  
Vol 14 (7) ◽  
pp. 991-998 ◽  
Author(s):  
Marco Cattaruzza ◽  
Caroline Dimigen ◽  
Hannelore Ehrenreich ◽  
Markus Hecker
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Muscle Cells ◽  
Endothelin B Receptor ◽  
Endothelin B

scholarly journals 247 Contractile Endothelin B Receptors on the Smooth Muscle Cells of the Human Umbilical Vein

2005 ◽  
Vol 58 (2) ◽  
pp. 397-397
Author(s):  
E Mildenberger ◽  
B Biesel ◽  
G Siegel ◽  
H V Versmold
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Umbilical Vein ◽  
Muscle Cells ◽  
Human Umbilical Vein ◽  
Endothelin B

scholarly journals Exosomal MFGE8 from high glucose induced endothelial cells is involved in calcification/senescence of vascular smooth muscle cells

2021 ◽  
Author(s):  
Yu-Qing Ni ◽  
Shuang Li ◽  
Xiao Lin ◽  
Yan-Jiao Wang ◽  
Jie-Yu He ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Calcification ◽  
Vascular Smooth Muscle Cells ◽  
High Glucose ◽  
Milk Fat ◽  
Umbilical Vein ◽  
Muscle Cells

AbstractVascular calcification/aging is a crucial feature of diabetic macro vasculopathy, resulting in serious cardiovascular diseases. The calcification/senescence of vascular smooth muscle cells (VSMCs) induced by hyperglycemia can cause diabetic vascular calcification/aging. However, the mechanism of VSMCs calcification/senescence involved in diabetic vascular calcification/aging remains unknown. The purpose of this study was to determine how the high glucose (HG) information in circulating blood is transmitted from vascular endothelial cells (ECs) to VSMCs, which are not contacted with blood directly. Exosomes have attracted much attention for their vital roles in regulating cell-to-cell communication. In this study, we found that milk fat globule epidermal growth factor 8 (MFGE8) was enriched in high glucose induced human umbilical vein endothelial cell exosomes (HG-HUVEC-Exo) and regulate VSMCs calcification/senescence, characterized by up-regulated expressions of alkaline phosphatase (ALP) and Runt-related transcription factor 2 (Runx2), as well as the increased mineralized nodules and senescence-associated β-galactosidase (SA-β-gal) positive cells. Upstream mechanism studies showed that sirtuin1 (SIRT1) was involved in VSMCs calcification/senescence by affecting the expression of MFGE8. We also found that inflammatory response mediated by IL-1β, IL-6, and IL-8 was closely associated with MFGE8 and played a key role in regulating HG-HUVEC-Exo-induced VSMCs calcification/senescence. These findings provide a new insight into the mechanism of exosomal MFGE8 as a potential preventive and therapeutic target for the intervention of diabetic vascular calcification/aging.

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