scholarly journals Physical contact between human vascular endothelial and smooth muscle cells modulates cytosolic and nuclear calcium homeostasis

2018 ◽  
Vol 96 (7) ◽  
pp. 655-661
Author(s):  
Ghada S. Hassan ◽  
Danielle Jacques ◽  
Pedro D’Orléans-Juste ◽  
Sheldon Magder ◽  
Ghassan Bkaily
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Culture Medium ◽  
Vascular Endothelial Cells ◽  
Muscle Cells ◽  
Cell Types ◽  
Physical Contact ◽  
Vascular Endothelial ◽  
Nuclear Calcium ◽  
Calcium Dependent

The interaction between vascular endothelial cells (VECs) and vascular smooth muscle cells (VSMCs) plays an important role in the modulation of vascular tone. There is, however, no information on whether direct physical communication regulates the intracellular calcium levels of human VECs (hVECs) and (or) human VSMCs (hVSMCs). Thus, the objective of the study is to verify whether co-culture of hVECs and hVSMCs modulates cytosolic ([Ca2+]c) and nuclear calcium ([Ca2+]n) levels via physical contact and (or) factors released by both cell types. Quantitative 3D confocal microscopy for [Ca2+]c and [Ca2+]n measurement was performed in cultured hVECs or hVSMCs or in co-culture of hVECs–hVSMCs. Our results show that: (1) physical contact between hVECs–hVECs or hVSMCs–hVSMCs does not affect [Ca2+]c and [Ca2+]n in these 2 cell types; (2) physical contact between hVECs and hVSMCs induces a significant increase only of [Ca2+]n of hVECs without affecting the level of [Ca2+]c and [Ca2+]n of hVSMCs; and (3) preconditioned culture medium of hVECs or hVSMCs does not affect [Ca2+]c and [Ca2+]n of both types of cells. We concluded that physical contact between hVECs and hVSMCs only modulates [Ca2+]n in hVECs. The increase of [Ca2+]n in hVECs may modulate nuclear functions that are calcium dependent.

Cell type specific electrophoretic polypeptide profiles of cultured bovine cells

1984 ◽  
Vol 72 (1) ◽  
pp. 135-145
Author(s):  
D.W. Lincoln ◽  
K.I. Braunschweiger ◽  
W.R. Braunschweiger ◽  
J.R. Smith
Keyword(s):  
Smooth Muscle ◽  
Pulmonary Artery ◽  
Smooth Muscle Cells ◽  
Vascular Endothelial Cells ◽  
Muscle Cells ◽  
Cell Types ◽  
Vascular Endothelial ◽  
Molecular Weights ◽  
Cell Type Specific ◽  
Electrophoretic Techniques

The polypeptide profiles of bovine vascular endothelial cells (from pulmonary artery and descending aorta), smooth muscle cells (from pulmonary artery) and fibroblast cells (from skin and lung) were examined by high-resolution two-dimensional polyacrylamide gel electrophoretic techniques. A set of polypeptides (molecular weights between 43 X 10(3) and 47 X 10(3) and pI values from 6.0-4.8, respectively) exhibited patterns that were unique to the three cell types. In the case of smooth muscle cells, these polypeptides exhibited cell-density-dependent expression. These results allow for identification of the three cell types on the basis of their highly specific polypeptide signatures.

scholarly journals Inhibitory effect of caveolin-1 in vascular endothelial cells, pericytes and smooth muscle cells

Oncotarget ◽  
2017 ◽  
Vol 8 (44) ◽  
pp. 76165-76173 ◽  
Author(s):  
Hongping Xu ◽  
Liwei Zhang ◽  
Wei Chen ◽  
Jiazhou Xu ◽  
Ruting Zhang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Endothelial Cells ◽  
Muscle Cells ◽  
Inhibitory Effect ◽  
Vascular Endothelial ◽  
Caveolin 1

scholarly journals IL-8 reduces VCAM-1 secretion of smooth muscle cells by increasing p-ERK expression when 3-D co-cultured with vascular endothelial cells

2011 ◽  
Vol 34 (3) ◽  
pp. 138 ◽  
Author(s):  
Zhi Zhang ◽  
Guang Chu ◽  
Hong-Xian Wu ◽  
Ni Zou ◽  
Bao-Gui Sun ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Type I Collagen ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Muscle Cells ◽  
Type I ◽  
Vascular Endothelial ◽  
Culture Model

Objective: The goal of this study was to investigate the crosstalk between vascular endothelial cells (ECs) and smooth muscle cells (SMCs) using a three-dimensional (3-D) co-culture model. In addition, the role of IL-8 in this crosstalk was investigated. Methods: A 3-D co-culture model was constructed using a Transwell chamber system and type I collagen gel. Human umbilical artery smooth muscle cells (HUASMCs) were suspended in the gel and added to the upper compartment of the Transwell. Human umbilical vein endothelial cells (HUVECs) were then grown on the surface of the gel. The growth of HUASMCs was tested with a CFDA SE cell proliferation kit. IL-8 and other bioactive substances were investigated by ELISA and real-time PCR. The alteration of p-ERK expression related to the change in IL-8 levels was also examined by Western blot analysis. Results: The proliferation rate of HUASMCs in the 3-D co-culture model was 0.679 ± 0.057. Secretion and transcription of VEGF, t-PA, NO and VCAM-1 in the 3-D co-culture model were different than in single (2-D) culture. When 3-D co-cultured, IL-8 released by HUVECs was significantly increased (2.35 ± 0.16 fold) (P﹤0.05) and the expression of VCAM-1 from HUASMCs was reduced accordingly (0.55±0.09 fold). In addition, increasing or decreasing the level of IL-8 changed the level of p-ERK and VCAM-1 expression. The reduction of VCAM-1, resulting from increased IL-8, could be blocked by the MEK inhibitor, PD98059. Conclusion: Crosstalk between HUVECs and HUASMCs occurred and was probably mediated by IL-8 in this 3-D co-culture model.

Regulation Of Vascular Prostacyclin (PGI2) Synthesis

1981 ◽  
Author(s):  
S Coughlin ◽  
M Moskowitz ◽  
H N Antoniades ◽  
L Levine
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Muscle Cells ◽  
Cell Types ◽  
Feedback Mechanism ◽  
Vascular Endothelial ◽  
Serum Factor ◽  
Negative Feedback Mechanism ◽  
Cells In Culture ◽  
Other Substances

We have examined the possibility that substances released during platelet degranulation modify vascular PGI2 synthesis. PGI2 is a potent inhibitor of platelet function produced by vascular endothelial and smooth muscle cells. Regulation of PGI2 synthesis by blood vessels is not well understood. We report that a platelet- dependent factor in serum dramatically stimulates PGI2 synthesis by vascular endothelial and smooth muscle cells in culture. We further report that platelet-derived growth factor (PDGF), a releasable protein found in platelet alpha granules, stimulates PGI2 synthesis by the above cell types by over 100 fold. The concentration of PDGF required to elicit this effect is below that reported in human serum. The above mentioned serum factor is relatively heat stable, non-dialyzable, and cationic; preliminary studies indicate that anti-PDGF antiserum is capable of blocking stimulation of PGI2 synthesis by both PDGF and serum. These data suggest that the serum factor may indeed be PDGF. PDGF acts synergistically with other platelet granule constituents (serotonin, ATP) and with thrombin to stimulate PGI2 synthesis by vascular cells in culture. We thus postulate that platelet-released PDGF, in concert with other substances generated during clotting, acts to increase vessel wall PGI2 synthesis as part of a negative feedback mechanism controlling platelet aggregation. A defect in the ability of a blood vessel to increase PGI2 production in response to platelet degranulation, as may occur in atherosclerotic vessels, could perhaps contribute to the genesis of thromboembolic events.

Sign in / Sign up

Export Citation Format

Share Document