MODULATION OF SECRETION OF VASOACTIVE MATERIALS FROM HUMAN AND BOVINEENDOTHELIAL-CELLS BY CYCLIC STRAIN

Citation
Ja. Carosi et al., MODULATION OF SECRETION OF VASOACTIVE MATERIALS FROM HUMAN AND BOVINEENDOTHELIAL-CELLS BY CYCLIC STRAIN, Biotechnology and bioengineering, 43(7), 1994, pp. 615-621
Citations number
49
Categorie Soggetti
Biothechnology & Applied Migrobiology
ISSN journal
00063592
Volume
43
Issue
7
Year of publication
1994
Pages
615 - 621
Database
ISI
SICI code
0006-3592(1994)43:7<615:MOSOVM>2.0.ZU;2-Z
Abstract
The effects of cyclical expansion and relaxation of the vessel wall on endothelial cell metabolism have been modeled using a uniaxial strain device and cultured endothelial cell monolayers. Also, the effects of stopping and then restarting cyclic strain on metabolite secretion ra tes were determined. Secretion rates of prostacyclin (PGl(2)), endothe lin, tissue plasminogen activator (t-PA), and plasminogen activator in hibitor-type 1 (PAl-1) by endothelial cells were constant over 24-h pe riods. The secretion of both PGl(2) and endothelin was enhanced in cel ls exposed to high physiological levels of cyclical strain (10% at 1 H z) compared with controls, while t-PA production was unaltered. These results were true for both human and bovine endothelial cells. Charact erization of the response of human endothelial cells to cyclical strai n made evaluation of stretch effects on PAl-1 secretion possible. A ne arly twofold increase in PAl-1 secretion by cells exposed to arterial levels of strain was observed. Endothelin secretion remained elevated even after strain was stopped for 12 h, while PGl(2) secretion returne d to control values upon cessation of cyclic stretch. These results in dicate that physiological levels of cyclic mechanical strain can signi ficantly modulate secretion of vasoactive metabolites from endothelial cells. The changes seen in secretion are, in some cases, quite differ ent from those caused by arterial levels of fluid shear stress exposur e. (C) 1994 John Wiley and Sons, Inc.