Cell Adhesion Regulates the Plasminogen Activator Inhibitor-1 Gene Expression in Anchorage-Dependent Cells

2002 ◽  
Vol 291 (1) ◽  
pp. 185-190 ◽  
Author(s):  
Chun-Chung Lee ◽  
Kou-Gi Shyu ◽  
Shankung Lin ◽  
Bao-Wei Wang ◽  
Ya-Chen Liu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Adhesion ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor

Bezafibrate Induces Plasminogen Activator Inhibitor-1 Gene Expression in a CLOCK-Dependent Circadian Manner

2010 ◽  
Vol 78 (1) ◽  
pp. 135-141 ◽  
Author(s):  
Katsutaka Oishi ◽  
Satoru Koyanagi ◽  
Naoya Matsunaga ◽  
Koji Kadota ◽  
Eriko Ikeda ◽  
...  
Keyword(s):  
Gene Expression ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor

Early genetic responses in rat vascular tissue after simulated diving

2012 ◽  
Vol 44 (24) ◽  
pp. 1201-1207 ◽  
Author(s):  
Ingrid Eftedal ◽  
Arve Jørgensen ◽  
Ragnhild Røsbjørgen ◽  
Arnar Flatberg ◽  
Alf O. Brubakk
Keyword(s):  
Gene Expression ◽  
Transcription Factor ◽  
Plasminogen Activator ◽  
Differential Gene Expression ◽  
Vascular Function ◽  
Plasminogen Activator Inhibitor ◽  
Fine Tuning ◽  
Plasminogen Activator Inhibitor 1 ◽  
Differential Gene ◽  
Activator Inhibitor

Diving causes a transient reduction of vascular function, but the mechanisms behind this are largely unknown. The aim of this study was therefore to analyze genetic reactions that may be involved in acute changes of vascular function in divers. Rats were exposed to 709 kPa of hyperbaric air (149 kPa Po2) for 50 min followed by postdive monitoring of vascular bubble formation and full genome microarray analysis of the aorta from diving rats ( n = 8) and unexposed controls ( n = 9). Upregulation of 23 genes was observed 1 h after simulated diving. The differential gene expression was characteristic of cellular responses to oxidative stress, with functions of upregulated genes including activation and fine-tuning of stress-responsive transcription, cytokine/cytokine receptor signaling, molecular chaperoning, and coagulation. By qRT-PCR, we verified increased transcription of neuron-derived orphan receptor-1 ( Nr4a3), plasminogen activator inhibitor 1 ( Serpine1), cytokine TWEAK receptor FN14 ( Tnfrsf12a), transcription factor class E basic helix-loop-helix protein 40 ( Bhlhe40), and adrenomedullin ( Adm). Hypoxia-inducible transcription factor HIF1 subunit HIF1-α was stabilized in the aorta 1 h after diving, and after 4 h there was a fivefold increase in total protein levels of the procoagulant plasminogen activator inhibitor 1 (PAI1) in blood plasma from diving rats. The study did not have sufficient power for individual assessment of effects of hyperoxia and decompression-induced bubbles on postdive gene expression. However, differential gene expression in rats without venous bubbles was similar to that of all the diving rats, indicating that elevated Po2 instigated the observed genetic reactions.

Activation of Plasminogen Activator Inhibitor-1 Synthesis by Phorbol Esters in Human Promyelocyte HL-60

1999 ◽  
Vol 81 (03) ◽  
pp. 415-422 ◽  
Author(s):  
Sophie Lopez ◽  
Franck Peiretti ◽  
Pierre Morange ◽  
Amale Laouar ◽  
Chantal Fossat ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Adhesion ◽  
Protein Kinase ◽  
Plasminogen Activator ◽  
Specific Inhibitor ◽  
Plasminogen Activator Inhibitor ◽  
Transduction Pathway ◽  
Protein Levels ◽  
Activator Inhibitor ◽  
Pai 1

SummaryHL-60 cells treated by PMA develop the monocyte adherent pheno-type and synthesize plasminogen activator inhibitor type-1 (PAI-1). We focused our study on the identification of the PMA-activated protein kinase C (PKC) isoform and its downstream transduction pathway activating PAI-1 synthesis. Acquisition of the monocytic phenotype was evidenced by cell adherence (90-95%) and a sharp increase of CD 36 and receptor for urokinase plasminogen activator (uPAR) surface expression. Ro 31-8220, a specific inhibitor of PKC, prevented PMA-induced PAI-1 synthesis (mRNA and protein levels) and cell adhesion. To identify the PKC isoform, we took advantage of the HL-525 cell line, an HL-60 cell variant deficient in PKCβ gene expression. This defect prevents PMA to induce the differentiation process. HL-525 stimulated by PMA did not synthesize PAI-1 nor become adherent. However, in HL-525 cells either pretreated by retinoic acid that reinduces PKCβ gene expression or transfected with PKCβ cDNA, PMA significantly activated PAI-1 synthesis and adhesion of cells. Immunoblotting of active Mitogen Activated Protein Kinase (MAPK) p42/p44 in HL-60 cells showed a preferential and sustained activation of the p42 isoform by PMA over the p44 isoform. Ro 31-8220 significantly attenuated this activation. PD 098059 and U0126, both highly specific MEK inhibitors, efficiently prevented PMA-induced PAI-1 synthesis (mRNA and protein levels) and cell adhesion whereas SB203580, a specific inhibitor of stress-activated MAPK p38, did not. Results obtained from HL-60 and HL-525 cells indicate that the PMA-activated transduction pathway of uPAR expression involves a PKC isoform other than PKCβ.In conclusion, we propose that the pathway PKCβ-MEK-MAPK p42 is a potential linear route for PAI-1 synthesis leading to morphological changes and adherence linked to PMA-induced differentiation in HL-60 cells.

scholarly journals The active conformation of plasminogen activator inhibitor 1, a target for drugs to control fibrinolysis and cell adhesion

Structure ◽  
1999 ◽  
Vol 7 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Allan M Sharp ◽  
Penelope E Stein ◽  
Navraj S Pannu ◽  
Robin W Carrell ◽  
Mitchell B Berkenpas ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Plasminogen Activator ◽  
Plasminogen Activator Inhibitor ◽  
Active Conformation ◽  
Plasminogen Activator Inhibitor 1 ◽  
Activator Inhibitor
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