scholarly journals Suppression of Proteoglycan Synthesis by Calcium Ionophore A23187 in Cultured Vascular Endothelial Cells: Implication of Intracellular Calcium Accumulation in Lead Inhibition of Endothelial Proteoglycan Synthesis

2002 ◽  
Vol 48 (5) ◽  
pp. 460-466 ◽  
Author(s):  
Yasuyuki Fujiwara ◽  
Toshiyuki Kaji
Keyword(s):  
Endothelial Cells ◽  
Intracellular Calcium ◽  
Vascular Endothelial Cells ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Proteoglycan Synthesis ◽  
Ionophore A23187 ◽  
Vascular Endothelial ◽  
Calcium Accumulation

Calcium, calmodulin, and the production of prostacyclin by cultured vascular endothelial cells

1983 ◽  
Vol 3 (11) ◽  
pp. 1007-1015 ◽  
Author(s):  
J. M. Seid ◽  
S. Macneil ◽  
S. Tomlinson
Keyword(s):  
Endothelial Cells ◽  
Vascular Endothelial Cells ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Vascular Endothelial ◽  
Calmodulin Antagonist ◽  
Aortic Endothelial Cells ◽  
Intracellular Calcium Mobilization ◽  
Porcine Aortic Endothelial Cells

The production of prostacyclin (PGI2) by cultured porcine aortic endothelial cells, in response to serum and the calcium ionophore A23187, was inhibited by TMB-8, an antagonist of intracellular calcium mobilization. The calcium-channel blocker methoxyverapamil (D600) inhibited serum-induced PGI2 production in but had little effect on A23187-induced PGI2 production. Calmodulin activity was detected in endothelial-cell Jysates and was inhibited by the calmodulin antagonist W7, which also inhibited PGI2 production in response to both agonists. Calcium and calmodulin appear to play an important role in mediating PGI2 production by the vascular endothelium.

scholarly journals Rapid ultrastructural changes in the dense tubular system following platelet activation

Blood ◽  
1992 ◽  
Vol 80 (3) ◽  
pp. 718-723 ◽  
Author(s):  
L Ebbeling ◽  
C Robertson ◽  
A McNicol ◽  
JM Gerrard
Keyword(s):  
Intracellular Calcium ◽  
Platelet Activation ◽  
Calcium Ionophore ◽  
Cytosolic Calcium ◽  
Calcium Ionophore A23187 ◽  
Ultrastructural Changes ◽  
Ionophore A23187 ◽  
Tubular System ◽  
Protein Kinase C Activators ◽  
Morphologic Changes

Abstract The dense tubular system (DTS) functions to regulate platelet activation by sequestering or releasing calcium, similar to the sarcotubules of skeletal muscle. In resting platelets, the DTS exists as thin elongated membranes. Within 10 seconds of the addition of thrombin, platelets show a major ultrastructural change in their DTS: from the thin elongated form to a rounded vesicular form. These morphologic changes were demonstrated with two different stains and two different fixation methods. Platelets exposed to the calcium ionophore A23187 showed the same ultrastructural changes in the DTS. In contrast, the DTS remains in a thin elongated form when platelets are stimulated by the protein kinase C activators phorbol 12-myristate 13-acetate (PMA) and oleoylacetylglycerol (OAG). These morphologic changes may be related to the discharge of calcium from the DTS because this is stimulated by thrombin and A23187, but not by PMA. Preincubation of the platelets with the intracellular calcium chelator 5,5′-dimethyl-bis-(0- aminophenoxy)-ethane-N,N,N′,N tetra acetic acid (BAPTA) largely prevented both the thrombin-induced rise in intracellular calcium and the changes in DTS morphology, suggesting that the changes in DTS morphology are secondary to the increase in cytosolic calcium. The results provide a morphologic correlate to existing biochemical evidence showing that the DTS is involved early during paltelet activation.

Thrombin receptor 14-amino acid peptide binds to endothelial cells and stimulates calcium transients

1992 ◽  
Vol 263 (5) ◽  
pp. L595-L601 ◽  
Author(s):  
C. Tiruppathi ◽  
H. Lum ◽  
T. T. Andersen ◽  
J. W. Fenton ◽  
A. B. Malik
Keyword(s):  
Endothelial Cells ◽  
Intracellular Calcium ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Calcium Transients ◽  
Cell Protein ◽  
Affinity Constant ◽  
Thrombin Receptor ◽  
Vascular Endothelial ◽  
Amino Terminal

We examined the binding characteristics of the recently described thrombin receptor amino-terminal peptide, SFLLRNPNDKYEPF (T. K. H. Vu, D. T. Hung, V. I. Wheaton, and S. R. Coughlin. Cell 64: 1057-1068, 1991), termed TRP-14, and its effect in activating intracellular calcium transients in pulmonary vascular endothelial cells. Binding of 125I-labeled TRP-14 was found to be saturable with a affinity constant of 2 microM and maximum binding of 41 pmol/mg of cell protein. The 125I-labeled TRP-14 also interacted with bovine pulmonary microvessel endothelial cells, human umbilical vein endothelial cells, and porcine pulmonary artery smooth muscle cells. Binding of 125I-labeled diisopropylphosphoryl (DIP)-alpha-thrombin, which is catalytically inactive but binds to thrombin receptors, was not inhibited by TRP-14 or vice versa, indicating that TRP-14 did not compete for the alpha-thrombin binding site(s) on the endothelial cell surface. TRP-14 (> 1 microM) increased the concentration of intracellular calcium ([Ca2+]i) in endothelial cells with kinetics similar to the increase in [Ca2+]i triggered by alpha-thrombin. In contrast, DIP-alpha-thrombin did not increase [Ca2+]i and also did not prevent the rise in [Ca2+]i induced by the subsequent challenge with either TRP-14 or alpha-thrombin. Because the generation of TRP-14 by the proteolytically active forms of thrombin stimulated a rise in endothelial [Ca2+]i, TRP-14 may be the agonist responsible for the activation of the alpha-thrombin receptor in pulmonary vascular endothelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Is a rise in intracellular concentration of free calcium necessary or sufficient for stimulated cytoskeletal-associated actin?

1986 ◽  
Vol 102 (4) ◽  
pp. 1459-1463 ◽  
Author(s):  
R I Sha'afi ◽  
J Shefcyk ◽  
R Yassin ◽  
T F Molski ◽  
M Volpi ◽  
...  
Keyword(s):  
Intracellular Calcium ◽  
Pertussis Toxin ◽  
Incubation Medium ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Extracellular Calcium ◽  
Intracellular Concentration ◽  
The Other ◽  
Free Calcium ◽  
Ionophore A23187

The addition of the calcium ionophore A23187 to rabbit neutrophils increases the amount of actin associated with the cytoskeleton regardless of the presence or absence of calcium in the incubation medium. In the presence of extracellular calcium, the effect of A23187 is biphasic with respect to concentration. The action of the ionophore is rapid, transient, and is inhibited by pertussis toxin, hyperosmolarity, and quinacrine. On the other hand, the addition of pertussis toxin or hyperosmolarity has small if any, effect on the rise in intracellular calcium produced by A23187. While quinacrine does not affect the fMet-Leu-Phe-induced increase in cytoskeletal actin and the polyphosphoinositide turnover, its addition inhibits completely the stimulated increase in Ca-influx produced by the same stimulus. The results presented here suggest that a rise in the intracellular concentration of free calcium is neither necessary nor sufficient for the stimulated increase in cytoskeletal-associated actin. A possible relationship between the lipid remodeling stimulated by chemoattractants and the increased cytoskeletal actin is discussed.

The effects of HA compound calcium antagonists on delayed cerebral vasospasm in dogs

1986 ◽  
Vol 65 (1) ◽  
pp. 80-85 ◽  
Author(s):  
Masakazu Takayasu ◽  
Yoshio Suzuki ◽  
Masato Shibuya ◽  
Toshio Asano ◽  
Masahiko Kanamori ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Intracellular Calcium ◽  
Cerebral Vasospasm ◽  
Basilar Artery ◽  
Calcium Antagonists ◽  
Calcium Ionophore ◽  
Calcium Ionophore A23187 ◽  
Ionophore A23187 ◽  
Delayed Cerebral Vasospasm ◽  
Arterial Blood

✓ The authors have examined the effects of the HA compounds HA1004(N-(2-guanidinoethyl)-5-isoquino-linesulfonamide) and HA1077(l-(5-isoquinolinesulfonyl)homopiperazine), which are intracellular calcium antagonists, on delayed cerebral vasospasm from subarachnoid hemorrhage (SAH). The modes of action of these compounds were compared with those of the more commonly used calcium entry blockers. Calcium ionophore A23187 (4.8 × 10−6 M)-induced contraction of a canine basilar artery strip was completely antagonized by the HA compounds (10−5 M) but not by the entry-blocking calcium antagonists nicardipine, diltiazem, and verapamil (10−5 M), suggesting that the HA compounds act differently. Delayed cerebral vasospasm was induced by a “two-hemorrhage” canine model. The magnitude of the vasospasm and the effects of the HA compounds were determined angiographically. On SAH Day 7, a significant vasospasm was observed in every dog. The diameter of the basilar artery had diminished to 59% ± 2% (mean ± standard error) of the control value obtained before SAH (on Day 1). The intravenous administration of HA1004 caused a mild dilation of the basilar artery of 10% and 11% at doses of 3 and 10 mg/kg, respectively; however, HA1077 produced a more marked dilation of 19% and 27%, respectively, at the same doses. Both of these drugs lowered mean arterial blood pressure to about 80% and 50% at doses of 3 and 10 mg/kg, respectively. Intracisternal administration of the HA compounds (6 mg) completely reversed cerebral vasospasm without much effect on the blood pressure. The intracellular calcium antagonists of the HA compound group appear to be promising agents for the treatment of intractable cerebral vasospasm.

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