Human plasmin induces a receptor-mediated arachidonate release coupled with G proteins in endothelial cells

W. C. Chang, G. Y. Shi, Y. H. Chow, L. C. Chang, J. S. Hau, M. T. Lin, C. J. Jen, L. Y C Wing, H. L. Wu

研究成果: 雜誌貢獻文章

51 引文 (Scopus)

摘要

Treatment of cultured bovine carotid artery endothelial cells with 10-7 M plasmin increased arachidonate release coupled with the increase in prostacyclin production. The stimulatory effect of plasmin on arachidonate release could be divided into the early and late phases according to its calcium dependency and pertussis toxin sensitivity. The early phase of plasmin-induced arachidonate release was a calcium-dependent and pertussis toxin-sensitive response, which was observed within 20 min after plasmin treatment. The late phase was a calcium-independent and pertussis toxin- insensitive response, which was induced gradually from 20 to 60 min. Induction of the early phase of plasmin's effect required both the lysine binding and catalytic sites in plasmin molecule because it was inhibited either by the binding antagonist tranexamic acid or by the serine protease inhibitor aprotinin. Guanosine 5'-O-(2-thiotriphosphate) potentiated the effect of plasmin in permeabilized or nonpermeabilized cells, indicating that the early phase effect was mediated by a pertussis toxin-sensitive guanosine 5'-triphosphate (GTP)-binding protein. The late phase of plasmin's effect was due to the catalytic activity because it was inhibited by aprotinin but not by tranexamic acid. Microplasmin structurally having the catalytic sites induced a similar late phase effect. Plasmin did not elicit the metabolism of phosphatidyl polyphosphoinositides. These studies demonstrate that the activation of phospholipase A2, which results in arachidonate release, in the early phase of plasmin's effect is a receptor-mediation via GTP-binding protein that is not coupled through phospholipase C activation.

原文英語
期刊American Journal of Physiology - Cell Physiology
264
發行號2 33-2
出版狀態已發佈 - 1993
對外發佈Yes

指紋

Fibrinolysin
Endothelial cells
GTP-Binding Proteins
Endothelial Cells
Pertussis Toxin
Tranexamic Acid
Aprotinin
Guanosine
Guanosine Triphosphate
Calcium
Catalytic Domain
Carrier Proteins
Chemical activation
Phosphatidylinositol Phosphates
Serine Proteinase Inhibitors
Phospholipases A2
Type C Phospholipases
Epoprostenol
Carotid Arteries
Metabolism

ASJC Scopus subject areas

  • Cell Biology
  • Clinical Biochemistry
  • Physiology

引用此文

Human plasmin induces a receptor-mediated arachidonate release coupled with G proteins in endothelial cells. / Chang, W. C.; Shi, G. Y.; Chow, Y. H.; Chang, L. C.; Hau, J. S.; Lin, M. T.; Jen, C. J.; Wing, L. Y C; Wu, H. L.

於: American Journal of Physiology - Cell Physiology, 卷 264, 編號 2 33-2, 1993.

研究成果: 雜誌貢獻文章

Chang, WC, Shi, GY, Chow, YH, Chang, LC, Hau, JS, Lin, MT, Jen, CJ, Wing, LYC & Wu, HL 1993, 'Human plasmin induces a receptor-mediated arachidonate release coupled with G proteins in endothelial cells', American Journal of Physiology - Cell Physiology, 卷 264, 編號 2 33-2.
Chang, W. C. ; Shi, G. Y. ; Chow, Y. H. ; Chang, L. C. ; Hau, J. S. ; Lin, M. T. ; Jen, C. J. ; Wing, L. Y C ; Wu, H. L. / Human plasmin induces a receptor-mediated arachidonate release coupled with G proteins in endothelial cells. 於: American Journal of Physiology - Cell Physiology. 1993 ; 卷 264, 編號 2 33-2.
@article{5c9b291868924eb0b1d63c4fbbeb7e0d,
title = "Human plasmin induces a receptor-mediated arachidonate release coupled with G proteins in endothelial cells",
abstract = "Treatment of cultured bovine carotid artery endothelial cells with 10-7 M plasmin increased arachidonate release coupled with the increase in prostacyclin production. The stimulatory effect of plasmin on arachidonate release could be divided into the early and late phases according to its calcium dependency and pertussis toxin sensitivity. The early phase of plasmin-induced arachidonate release was a calcium-dependent and pertussis toxin-sensitive response, which was observed within 20 min after plasmin treatment. The late phase was a calcium-independent and pertussis toxin- insensitive response, which was induced gradually from 20 to 60 min. Induction of the early phase of plasmin's effect required both the lysine binding and catalytic sites in plasmin molecule because it was inhibited either by the binding antagonist tranexamic acid or by the serine protease inhibitor aprotinin. Guanosine 5'-O-(2-thiotriphosphate) potentiated the effect of plasmin in permeabilized or nonpermeabilized cells, indicating that the early phase effect was mediated by a pertussis toxin-sensitive guanosine 5'-triphosphate (GTP)-binding protein. The late phase of plasmin's effect was due to the catalytic activity because it was inhibited by aprotinin but not by tranexamic acid. Microplasmin structurally having the catalytic sites induced a similar late phase effect. Plasmin did not elicit the metabolism of phosphatidyl polyphosphoinositides. These studies demonstrate that the activation of phospholipase A2, which results in arachidonate release, in the early phase of plasmin's effect is a receptor-mediation via GTP-binding protein that is not coupled through phospholipase C activation.",
keywords = "plasmin, prostacyclin",
author = "Chang, {W. C.} and Shi, {G. Y.} and Chow, {Y. H.} and Chang, {L. C.} and Hau, {J. S.} and Lin, {M. T.} and Jen, {C. J.} and Wing, {L. Y C} and Wu, {H. L.}",
year = "1993",
language = "English",
volume = "264",
journal = "American Journal of Physiology",
issn = "0363-6143",
publisher = "American Physiological Society",
number = "2 33-2",

}

TY - JOUR

T1 - Human plasmin induces a receptor-mediated arachidonate release coupled with G proteins in endothelial cells

AU - Chang, W. C.

AU - Shi, G. Y.

AU - Chow, Y. H.

AU - Chang, L. C.

AU - Hau, J. S.

AU - Lin, M. T.

AU - Jen, C. J.

AU - Wing, L. Y C

AU - Wu, H. L.

PY - 1993

Y1 - 1993

N2 - Treatment of cultured bovine carotid artery endothelial cells with 10-7 M plasmin increased arachidonate release coupled with the increase in prostacyclin production. The stimulatory effect of plasmin on arachidonate release could be divided into the early and late phases according to its calcium dependency and pertussis toxin sensitivity. The early phase of plasmin-induced arachidonate release was a calcium-dependent and pertussis toxin-sensitive response, which was observed within 20 min after plasmin treatment. The late phase was a calcium-independent and pertussis toxin- insensitive response, which was induced gradually from 20 to 60 min. Induction of the early phase of plasmin's effect required both the lysine binding and catalytic sites in plasmin molecule because it was inhibited either by the binding antagonist tranexamic acid or by the serine protease inhibitor aprotinin. Guanosine 5'-O-(2-thiotriphosphate) potentiated the effect of plasmin in permeabilized or nonpermeabilized cells, indicating that the early phase effect was mediated by a pertussis toxin-sensitive guanosine 5'-triphosphate (GTP)-binding protein. The late phase of plasmin's effect was due to the catalytic activity because it was inhibited by aprotinin but not by tranexamic acid. Microplasmin structurally having the catalytic sites induced a similar late phase effect. Plasmin did not elicit the metabolism of phosphatidyl polyphosphoinositides. These studies demonstrate that the activation of phospholipase A2, which results in arachidonate release, in the early phase of plasmin's effect is a receptor-mediation via GTP-binding protein that is not coupled through phospholipase C activation.

AB - Treatment of cultured bovine carotid artery endothelial cells with 10-7 M plasmin increased arachidonate release coupled with the increase in prostacyclin production. The stimulatory effect of plasmin on arachidonate release could be divided into the early and late phases according to its calcium dependency and pertussis toxin sensitivity. The early phase of plasmin-induced arachidonate release was a calcium-dependent and pertussis toxin-sensitive response, which was observed within 20 min after plasmin treatment. The late phase was a calcium-independent and pertussis toxin- insensitive response, which was induced gradually from 20 to 60 min. Induction of the early phase of plasmin's effect required both the lysine binding and catalytic sites in plasmin molecule because it was inhibited either by the binding antagonist tranexamic acid or by the serine protease inhibitor aprotinin. Guanosine 5'-O-(2-thiotriphosphate) potentiated the effect of plasmin in permeabilized or nonpermeabilized cells, indicating that the early phase effect was mediated by a pertussis toxin-sensitive guanosine 5'-triphosphate (GTP)-binding protein. The late phase of plasmin's effect was due to the catalytic activity because it was inhibited by aprotinin but not by tranexamic acid. Microplasmin structurally having the catalytic sites induced a similar late phase effect. Plasmin did not elicit the metabolism of phosphatidyl polyphosphoinositides. These studies demonstrate that the activation of phospholipase A2, which results in arachidonate release, in the early phase of plasmin's effect is a receptor-mediation via GTP-binding protein that is not coupled through phospholipase C activation.

KW - plasmin

KW - prostacyclin

UR - http://www.scopus.com/inward/record.url?scp=0027529258&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0027529258&partnerID=8YFLogxK

M3 - Article

C2 - 8383426

AN - SCOPUS:0027529258

VL - 264

JO - American Journal of Physiology

JF - American Journal of Physiology

SN - 0363-6143

IS - 2 33-2

ER -