Dissociation between the Ca2+ signal and tube formation induced by vascular endothelial growth factor in bovine aortic endothelial cells

Junya Kawasaki, Katsuya Hirano, Mayumi Hirano, Junji Nishimura, Akio Nakatsuka, Masatoshi Fujishima, Hideo Kanaide

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

The correlation between the intracellular Ca2+ signal and the tube formation in collagen gels induced by vascular endothelial cell growth factor (VEGF) was investigated using cultured bovine aortic endothelial cells. The VEGF-induced sustained elevation of cytosolic Ca2+ concentration ([Ca2+](i)) was similarly inhibited by 10 μM 1-{β-[3-(4- methoxyphenyl)propyl]-4-methoxyphenethyl}-1H-imidazole hydrochloride (SKF 96365) and 10 μM troglitazone. However, 10 μM diltiazem had no effect. The basal tube formation obtained with 1% serum was augmented twofold by 100 ng/ml VEGF. SKF 96365 (0.1-10 μM) inhibited the VEGF-induced and basal tube formation, while 10 μM troglitazone or 10 μM diltiazem had no effect. The proliferation of endothelial cells was markedly inhibited by SKF 96365 but only slightly by troglitazone and diltiazem. The inhibition of tube formation by three Ca2+ entry blockers thus correlated with the inhibition of cell proliferation. The [Ca2+](i) elevation is thus not a prerequisite for VEGF to induce tube formation. (C) 2000 Elsevier Science B.V.

Original languageEnglish
Pages (from-to)19-29
Number of pages11
JournalEuropean Journal of Pharmacology
Volume398
Issue number1
DOIs
Publication statusPublished - Jun 9 2000
Externally publishedYes

Fingerprint

1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole
troglitazone
Vascular Endothelial Growth Factor A
Endothelial Cells
Diltiazem
Collagen
Gels
Cell Proliferation
Serum

All Science Journal Classification (ASJC) codes

  • Pharmacology

Cite this

Dissociation between the Ca2+ signal and tube formation induced by vascular endothelial growth factor in bovine aortic endothelial cells. / Kawasaki, Junya; Hirano, Katsuya; Hirano, Mayumi; Nishimura, Junji; Nakatsuka, Akio; Fujishima, Masatoshi; Kanaide, Hideo.

In: European Journal of Pharmacology, Vol. 398, No. 1, 09.06.2000, p. 19-29.

Research output: Contribution to journalArticle

Kawasaki, Junya ; Hirano, Katsuya ; Hirano, Mayumi ; Nishimura, Junji ; Nakatsuka, Akio ; Fujishima, Masatoshi ; Kanaide, Hideo. / Dissociation between the Ca2+ signal and tube formation induced by vascular endothelial growth factor in bovine aortic endothelial cells. In: European Journal of Pharmacology. 2000 ; Vol. 398, No. 1. pp. 19-29.
@article{e8c0029c7c9c4c05b12b4f5afe057bf7,
title = "Dissociation between the Ca2+ signal and tube formation induced by vascular endothelial growth factor in bovine aortic endothelial cells",
abstract = "The correlation between the intracellular Ca2+ signal and the tube formation in collagen gels induced by vascular endothelial cell growth factor (VEGF) was investigated using cultured bovine aortic endothelial cells. The VEGF-induced sustained elevation of cytosolic Ca2+ concentration ([Ca2+](i)) was similarly inhibited by 10 μM 1-{β-[3-(4- methoxyphenyl)propyl]-4-methoxyphenethyl}-1H-imidazole hydrochloride (SKF 96365) and 10 μM troglitazone. However, 10 μM diltiazem had no effect. The basal tube formation obtained with 1{\%} serum was augmented twofold by 100 ng/ml VEGF. SKF 96365 (0.1-10 μM) inhibited the VEGF-induced and basal tube formation, while 10 μM troglitazone or 10 μM diltiazem had no effect. The proliferation of endothelial cells was markedly inhibited by SKF 96365 but only slightly by troglitazone and diltiazem. The inhibition of tube formation by three Ca2+ entry blockers thus correlated with the inhibition of cell proliferation. The [Ca2+](i) elevation is thus not a prerequisite for VEGF to induce tube formation. (C) 2000 Elsevier Science B.V.",
author = "Junya Kawasaki and Katsuya Hirano and Mayumi Hirano and Junji Nishimura and Akio Nakatsuka and Masatoshi Fujishima and Hideo Kanaide",
year = "2000",
month = "6",
day = "9",
doi = "10.1016/S0014-2999(00)00296-X",
language = "English",
volume = "398",
pages = "19--29",
journal = "European Journal of Pharmacology",
issn = "0014-2999",
publisher = "Elsevier",
number = "1",

}

TY - JOUR

T1 - Dissociation between the Ca2+ signal and tube formation induced by vascular endothelial growth factor in bovine aortic endothelial cells

AU - Kawasaki, Junya

AU - Hirano, Katsuya

AU - Hirano, Mayumi

AU - Nishimura, Junji

AU - Nakatsuka, Akio

AU - Fujishima, Masatoshi

AU - Kanaide, Hideo

PY - 2000/6/9

Y1 - 2000/6/9

N2 - The correlation between the intracellular Ca2+ signal and the tube formation in collagen gels induced by vascular endothelial cell growth factor (VEGF) was investigated using cultured bovine aortic endothelial cells. The VEGF-induced sustained elevation of cytosolic Ca2+ concentration ([Ca2+](i)) was similarly inhibited by 10 μM 1-{β-[3-(4- methoxyphenyl)propyl]-4-methoxyphenethyl}-1H-imidazole hydrochloride (SKF 96365) and 10 μM troglitazone. However, 10 μM diltiazem had no effect. The basal tube formation obtained with 1% serum was augmented twofold by 100 ng/ml VEGF. SKF 96365 (0.1-10 μM) inhibited the VEGF-induced and basal tube formation, while 10 μM troglitazone or 10 μM diltiazem had no effect. The proliferation of endothelial cells was markedly inhibited by SKF 96365 but only slightly by troglitazone and diltiazem. The inhibition of tube formation by three Ca2+ entry blockers thus correlated with the inhibition of cell proliferation. The [Ca2+](i) elevation is thus not a prerequisite for VEGF to induce tube formation. (C) 2000 Elsevier Science B.V.

AB - The correlation between the intracellular Ca2+ signal and the tube formation in collagen gels induced by vascular endothelial cell growth factor (VEGF) was investigated using cultured bovine aortic endothelial cells. The VEGF-induced sustained elevation of cytosolic Ca2+ concentration ([Ca2+](i)) was similarly inhibited by 10 μM 1-{β-[3-(4- methoxyphenyl)propyl]-4-methoxyphenethyl}-1H-imidazole hydrochloride (SKF 96365) and 10 μM troglitazone. However, 10 μM diltiazem had no effect. The basal tube formation obtained with 1% serum was augmented twofold by 100 ng/ml VEGF. SKF 96365 (0.1-10 μM) inhibited the VEGF-induced and basal tube formation, while 10 μM troglitazone or 10 μM diltiazem had no effect. The proliferation of endothelial cells was markedly inhibited by SKF 96365 but only slightly by troglitazone and diltiazem. The inhibition of tube formation by three Ca2+ entry blockers thus correlated with the inhibition of cell proliferation. The [Ca2+](i) elevation is thus not a prerequisite for VEGF to induce tube formation. (C) 2000 Elsevier Science B.V.

UR - http://www.scopus.com/inward/record.url?scp=0034625652&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034625652&partnerID=8YFLogxK

U2 - 10.1016/S0014-2999(00)00296-X

DO - 10.1016/S0014-2999(00)00296-X

M3 - Article

VL - 398

SP - 19

EP - 29

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 1

ER -