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Cyclic strain-induced plasminogen activator inhibitor-1 (PAI-1) release from endothelial cells involves reactive oxygen species.

Abstract：

:The molecular mechanisms of the endothelial fibrinolytic activities modulated by mechanical strain are not clear. Endothelial cells (ECs) grown on a flexible membrane base were deformed with sinusoidal negative pressures to produce an average strain of 12%. Cyclic strain induced PAI-1 release in a time-dependent manner. Strain cells resulted in a 5-fold increase in PAI-1 release. Strain induced a sustained elevated level in intracellular reactive oxygen species (ROS). Concomitantly, a sustained increase of catalase activity was observed. Both ROS and catalase activity returned to basal levels with the removal of strain. ECs pretreated with antioxidant, N-acetyl-cysteine, abolished the strain-induced ROS generation as well as strained-induced PAI-1 release. Our results indicate that cyclic strain-induced PAI-1 secretion may be mediated by an increase in ROS generation and thus emphasizes the importance of intracellular ROS in the modulation of hemodynamic force-induced cellular response of ECs.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Cheng JJ,Chao YJ,Wung BS,Wang DL

doi

10.1006/bbrc.1996.1136

subject

Has Abstract

pub_date

1996-08-05 00:00:00

pages

100-5

issue

1

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(96)91136-5

journal_volume

225

pub_type

杂志文章

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