Calcium Channel Blockers Suppress Cytokine-induced Activation of Human Neutrophils

Shima, Etsuko; Katsube, Masataka; Kato, Takayuki; Kitagawa, Maki; Hato, Fumihiko; Hino, Masayuki; Takahashi, Tatsuji; Fujita, Hisakazu; Kitagawa, Seiichi

doi:10.1038/ajh.2007.13

Cited by 44 publications

(26 citation statements)

References 29 publications

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“…It was also reported that amlodipine but not verapamil or diltiazem showed antioxidant activity in membrane vesicles reconstituted from phospholipids (27). It was shown in human neutrophils that TNF-induced superoxide generation was significantly suppressed by amlodipine, nicardipine, cilnidipine, benidipine, efonidipine, nifedipine, and azelnidipine (5 -10 μ M), whereas it was not affected by verapamil or diltiazem (25). Furthermore, amlodipine and benidipine, but not nifedipine or diltiazem, induced NO synthesis in dog coronary microvessel ECs (28,29).…”

Section: Discussionmentioning

confidence: 92%

“…In the present study, we confirmed that CV-159 (10 μ M) significantly inhibited TNF-induced expression of e-selectin but not VCAM-1 or ICAM-1 expression in HUVECs. It was previously reported that nicardipine, amlodipine, and azelnidipine (10 μ M) failed to inhibit TNF-induced phosphorylation of p38 in human neutrophils (25). Furthermore, neither azelnidipine nor nifedipine inhibited H 2 O 2 -induced activation of p38 in rat neonatal cardiomyocytes (26).…”

Section: Discussionmentioning

confidence: 93%

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CV-159, a Unique Dihydropyridine Derivative, Prevents TNF-Induced Inflammatory Responses in Human Umbilical Vein Endothelial Cells

et al. 2010

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Abstract. CV-159, a 1,4-dihydropyridine derivative, has Ca 2+ antagonistic and anti-calmodulin actions. An early feature of atherosclerosis is vascular endothelial inflammatory change. We examined whether CV-159 has protective effects against endothelial inflammatory responses. After pretreatment of human umbilical vein endothelial cells (ECs) with CV-159 (10 μ M, 30 min), TNF-α (10 ng/ml) was applied for 20 min or 24 h. Expressions of inflammatory markers and activation of inflammatory signal molecules were examined by Western blotting. Reactive oxygen species (ROS) generation was examined by using 2′,7′-dichlorodihydrofluorescein diacetate. CV-159 inhibited TNF (24 h)-induced expression of e-selectin but not vascular cell adhesion molecule-1 and intercellular adhesion molecule-1. CV-159 inhibited TNF (20 min)-induced phosphorylation of JNK, p38, and NF-κ B p65 (Ser536). A JNK inhibitor, SP600125, and a p38 inhibitor, SB203580, inhibited TNF-induced e-selectin expression. An antioxidant drug, N -acetyl-L -cysteine (NAC), inhibited TNF-induced e-selectin expression. NAC inhibited TNF-induced phosphorylation of JNK and p38 but not NF-κ B. CV-159 inhibited TNF-induced ROS generation. Our results indicate that in ECs CV-159 specifically inhibits TNF-induced e-selectin expression through inhibition of JNK, p38, and NF-κ B phosphorylation. It is suggested that CV-159 prevents activation of JNK and p38 through inhibition of ROS, while it prevents activation of NF-κ B via a ROS-independent manner.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 93%

CV-159, a Unique Dihydropyridine Derivative, Prevents TNF-Induced Inflammatory Responses in Human Umbilical Vein Endothelial Cells

et al. 2010

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“…In subjects with juvenile AMI in whom we investigated plasma lipid peroxidation, expressed as TBARS, and plasma protein oxidation, expressed as carbonyl groups, a marked increase in both parameters was found at the initial stage of AMI [39,40]. The same behavior was present in AIS patients, in whom the increase in lipid peroxidation and protein oxidation, besides being evident at admission and 24 hours later [41], persisted for some months after the onset of AIS [42].…”

Section: Conclusive and Pharmacological Considerationmentioning

confidence: 82%

Fluidity and cytosolic Ca2+ concentration of circulating polymorphonuclear leukocytes at baseline in some chronic and acute clinical conditions: review of our survey

Caimi¹,

Canino²,

Presti³

et al. 2016

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Abstract. Objective: In this mini-review we describe the behavior of polymorphonuclear leukocyte (PMN) membrane fluidity and of PMN cytosolic Ca 2+ concentration in some chronic and acute clinical conditions. Methods: PMN membrane fluidity was evaluated employing the fluorescent probe Fura-2AM, and PMN cytosolic Ca 2+ concentration was evaluated using the fluorescent probe TMA-DPH. Results: From the determination of these two parameters investigated on resting PMNs, an almost constant increase in PMN cytosolic Ca 2+ concentration in chronic clinical conditions, such as vascular atherosclerotic disease with and without diabetes mellitus, essential hypertension, chronic kidney disease, and diabetes mellitus of both types, and a decrease in PMN membrane fluidity in acute clinical conditions, such as juvenile acute myocardial infarction and acute ischemic stroke, are evident. Conclusion: The possible reasons for this different behavior are analyzed on the basis of pathophysiological considerations.

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“…Both types of calcium channel antagonists were used to investigate which was the most important in this context. The high and low VGCCs were blocked using V + D (Shima et al, 2008), and 2-APB was used as a non-specific TRP cation channel blocker (Togashi et al, 2008;Nazıroglu et al, 2011a,b). The data from this study indicated that blockade of either VGCC or TRP had significant effects on neutrophil [Ca 2+ ] i response to fMLP, although VGCC blockade produced the largest reduction.…”

Section: Discussionmentioning

confidence: 99%

Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea

Kaplan

Nazıroğlu

Güney

et al. 2013

Journal of Reproductive Immunology

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Calcium Channel Blockers Suppress Cytokine-induced Activation of Human Neutrophils

Cited by 44 publications

References 29 publications

CV-159, a Unique Dihydropyridine Derivative, Prevents TNF-Induced Inflammatory Responses in Human Umbilical Vein Endothelial Cells

CV-159, a Unique Dihydropyridine Derivative, Prevents TNF-Induced Inflammatory Responses in Human Umbilical Vein Endothelial Cells

Fluidity and cytosolic Ca2+ concentration of circulating polymorphonuclear leukocytes at baseline in some chronic and acute clinical conditions: review of our survey

Non-steroidal anti-inflammatory drug modulates oxidative stress and calcium ion levels in the neutrophils of patients with primary dysmenorrhea

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