Expression patterns of sarco/endoplasmic reticulum Ca2+-ATPase and inositol 1,4,5-trisphosphate receptor isoforms in vascular endothelial cells

Cell Calcium ◽  
1999 ◽  
Vol 25 (5) ◽  
pp. 371-380 ◽  
Author(s):  
I. Mountian ◽  
V.G. Manolopoulos ◽  
H.De Smedt ◽  
J.B. Parys ◽  
L. Missiaen ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Endoplasmic Reticulum ◽  
Vascular Endothelial Cells ◽  
Expression Patterns ◽  
Vascular Endothelial ◽  
Receptor Isoforms ◽  
Inositol 1,4,5 Trisphosphate ◽  
Trisphosphate Receptor

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

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.

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 The related FLT4, FLT1, and KDR receptor tyrosine kinases show distinct expression patterns in human fetal endothelial cells.

1993 ◽  
Vol 178 (6) ◽  
pp. 2077-2088 ◽  
Author(s):  
A Kaipainen ◽  
J Korhonen ◽  
K Pajusola ◽  
O Aprelikova ◽  
M G Persico ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Growth Factor ◽  
Tyrosine Kinases ◽  
Receptor Tyrosine Kinases ◽  
Vascular Endothelial Cells ◽  
Expression Patterns ◽  
Vascular Endothelial ◽  
Vascular Permeability Factor ◽  
Kinase Gene ◽  
Permeability Factor

The growth factor receptors expressed on endothelial cells are of special interest because of their potential to program endothelial cell growth and differentiation during development and neovascularization in various pathological states, such as wound healing and angiogenesis associated with tumorigenesis. Vascular endothelial growth factor ([VEGF] also known as vascular permeability factor) is a potent mitogen and permeability factor, which has been suggested to play a role in embryonic and tumor angiogenesis. The newly cloned FLT4 receptor tyrosine kinase gene encodes a protein related to the VEGF receptors FLT1 and KDR/FLK-1. We have here studied the expression of FLT4 and the other two members of this receptor family in human fetal tissues by Northern and in situ hybridization. These results were also compared with the sites of expression of VEGF and the related placenta growth factor (PlGF). Our results reveal FLT4 mRNA expression in vascular endothelial cells in developing vessels of several organs. A comparison of FLT4, FLT1 and KDR/FLK-1 receptor mRNA signals shows overlapping, but distinct expression patterns in the tissues studied. Certain endothelia lack one or two of the three receptor mRNAs. These data suggest that the receptor tyrosine kinases encoded by the FLT gene family may have distinct functions in the regulation of the growth/differentiation of blood vessels.

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.

scholarly journals Reconciling VEGF With VPF: The Importance of Increased Vascular Permeability for Stroma Formation in Tumors, Healing Wounds, and Chronic Inflammation

2021 ◽  
Vol 9 ◽  
Author(s):  
Harold F. Dvorak
Keyword(s):  
Endothelial Cells ◽  
Connective Tissue ◽  
Vascular Permeability ◽  
Vascular Endothelial Cells ◽  
Inflammatory Diseases ◽  
Expression Patterns ◽  
Vascular Endothelial ◽  
Vascular Permeability Factor ◽  
Healing Wounds

It is widely believed that vascular endothelial growth factor (VEGF) induces angiogenesis by its direct mitogenic and motogenic actions on vascular endothelial cells. However, these activities are only detected when endothelial cells are cultured at very low (0.1%) serum concentrations and would not be expected to take place at the much higher serum levels found in angiogenic sites in vivo. This conundrum can be resolved by recalling VEGF’s original function, that of an extremely potent vascular permeability factor (VPF). In vivo VPF/VEGF increases microvascular permeability such that whole plasma leaks into the tissues where it undergoes clotting by tissue factor that is expressed on tumor and host connective tissue cells to deposit fibrin and generate serum. By providing tissue support and by reprogramming the gene expression patterns of cells locally, fibrin and serum can together account for the formation of vascular connective tissue stroma. In sum, by increasing vascular permeability, VPF/VEGF triggers the “wound healing response,” setting in motion a fundamental pathophysiological process that induces the mature stroma that is found not only in healing wounds but also in solid tumors and chronic inflammatory diseases. Once initiated by increased vascular permeability, this response may be difficult to impede, perhaps contributing to the limited success of anti-VEGF therapies in treating cancer.

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