scholarly journals Heterogeneity of caffeine- and bradykinin-sensitive Ca2+ stores in vascular endothelial cells

1994 ◽  
Vol 300 (3) ◽  
pp. 637-641 ◽  
Author(s):  
W F Graier ◽  
S Simecek ◽  
D K Bowles ◽  
M Sturek
Keyword(s):  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Coronary Artery ◽  
Right Coronary Artery ◽  
Functional Relationship ◽  
Functional Organization ◽  
Vascular Endothelial Cells ◽  
Transient Increase ◽  
Vascular Endothelial ◽  
Filling State

The filling state of Ca2+ stores in endothelial cells regulates Ca2+ entry. The functional relationship between the major Ca2+ stores [i.e. Ins(1,4,5)P3-sensitive (= bradykinin-sensitive stores, ‘BsS’) and caffeine-sensitive stores] is unknown. In pig right-coronary-artery endothelial cells, caffeine failed to release Ca2+ in 68% of the cells (quiet-responders), but increased bradykinin (Bk)-induced Ca2+ release 2.5-fold. In Bk-pre-stimulated cells, caffeine increased Ca2+ release upon a second stimulation with Bk 3.2-fold. In quiet-responders caffeine alone did not affect net Ca2+ storage, whereas Bk or caffeine followed by Bk decreased the intracellular Ca2+ pool to 45% and 15%, respectively. Blockade of the endoplasmic-reticulum Ca2+ pump by thapsigargin unmasked the effect of caffeine in quiet-responders, resulting in a transient increase in intracellular free Ca2+ concentration ([Ca2+]i). In 37% of the cells caffeine alone transiently increased [Ca2+]i and depleted BsS. This study suggests a heterogeneity in functional organization of endothelial Ca2+ stores. In quiet-responders, caffeine translocates Ca2+ towards the BsS, whereas in overt-responders caffeine empties the BsS.

scholarly journals Regulation of capillary tubules and lipid formation in vascular endothelial cells and macrophages via extracellular vesicle-mediated microRNA-4306 transfer

2018 ◽  
Vol 47 (1) ◽  
pp. 453-469 ◽  
Author(s):  
Ying Yang ◽  
Hui Luo ◽  
Can Zhou ◽  
Rongyi Zhang ◽  
Si Liu ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Coronary Artery ◽  
Vascular Endothelial Cells ◽  
Density Lipoprotein ◽  
Extracellular Vesicle ◽  
Luciferase Reporter ◽  
Vascular Endothelial ◽  
Human Coronary Artery ◽  
Lipid Formation

Objective This study aimed to examine regulation of capillary tubules and lipid formation in vascular endothelial cells and macrophages via extracellular vesicle-mediated microRNA (miRNA)-4306 transfer Methods Whole blood samples (12 mL) were collected from 53 patients, and miR-4306 levels in extracellular vesicles (EVs) were analyzed by reverse transcription-polymerase chain reaction. Human coronary artery vascular endothelial cells (HCAECs) and human monocyte-derived macrophages (HMDMs) were transfected with a scrambled oligonucleotide, an miR-4306 mimic, or an anti-miR-4306 inhibitor. The direct effect of miR-4306 on the target gene was analyzed by a dual-luciferase reporter assay. Results EV-contained miR-4306 released from HMDMs was significantly upregulated in coronary artery disease. Oxidized low-density lipoprotein (ox-LDL)-stimulated HMDM-derived EVs inhibited proliferation, migration, and angiogenesis abilities of HCAECs in vitro. However, ox-LDL-stimulated HCAEC-derived EVs enhanced lipid formation of HMDMs. The possible mechanism of these findings was partly due to EV-mediated miR-4306 upregulation of the Akt/nuclear factor kappa B signaling pathway. Conclusions Paracrine cellular crosstalk between HCAECs and HMDMs probably supports the pro-atherosclerotic effects of EVs under ox-LDL stress.

Icariin protects vascular endothelial cells from oxidative stress through inhibiting endoplasmic reticulum stress

2019 ◽  
Vol 17 (3) ◽  
pp. 205-212 ◽  
Author(s):  
Fang-yuan Wang ◽  
Jian Jia ◽  
Huan-huan Song ◽  
Cheng-ming Jia ◽  
Chang-bo Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

scholarly journals Na +/Ca2+ exchangers and Orai channels jointly refill endoplasmic reticulum (ER) Ca2+ via ER nanojunctions in vascular endothelial cells

2017 ◽  
Vol 469 (10) ◽  
pp. 1287-1299 ◽  
Author(s):  
Cristiana M. L. Di Giuro ◽  
Niroj Shrestha ◽  
Roland Malli ◽  
Klaus Groschner ◽  
Cornelis van Breemen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Orai Channels

cGMP stimulates endoplasmic reticulum Ca2+-ATPase in vascular endothelial cells

Life Sciences ◽  
2003 ◽  
Vol 73 (16) ◽  
pp. 2019-2028 ◽  
Author(s):  
Kin-Ling Lau ◽  
Siu-Kai Kong ◽  
Wing-Hung Ko ◽  
Hiu-Yee Kwan ◽  
Yu Huang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial

scholarly journals Microtubules and the endoplasmic reticulum are highly interdependent structures.

1986 ◽  
Vol 103 (4) ◽  
pp. 1557-1568 ◽  
Author(s):  
M Terasaki ◽  
L B Chen ◽  
K Fujiwara
Keyword(s):  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Intermediate Filaments ◽  
Vascular Endothelial Cells ◽  
Staining Technique ◽  
Vascular Endothelial ◽  
Extended State ◽  
Short Term ◽  
Dye Staining ◽  
Prolonged Absence

The interrelationships of the endoplasmic reticulum (ER), microtubules, and intermediate filaments were studied in the peripheral regions of thin, spread fibroblasts, epithelial, and vascular endothelial cells in culture. We combined a fluorescent dye staining technique to localize the ER with immunofluorescence to localize microtubules or intermediate filaments in the same cell. Microtubules and the ER are sparse in the lamellipodia, but intermediate filaments are usually completely absent. These relationships indicate that microtubules and the ER advance into the lamellipodia before intermediate filaments. We observed that microtubules and tubules of the ER have nearly identical distributions in lamellipodia, where new extensions of both are taking place. We perturbed microtubules by nocodazole, cold temperature, or hypotonic shock, and observed the effects on the ER distribution. On the basis of our observations in untreated cells and our experiments with microtubule perturbation, we conclude that microtubules and the ER are highly interdependent in two ways: (a) polymerization of individual microtubules and extension of individual ER tubules occur together at the level of resolution of the fluorescence microscope, and (b) depolymerization of microtubules does not disrupt the ER network in the short term (15 min), but prolonged absence of microtubules (2 h) leads to a slow retraction of the ER network towards the cell center, indicating that over longer periods of time, the extended state of the entire ER network requires the microtubule system.

Sign in / Sign up

Export Citation Format

Share Document