Induction of plasminogen activator inhibitor-1 in endothelial cells by basic fibroblast growth factor and its modulation by fibric acid. 2002

Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan.

Plasminogen activator inhibitor-1 (PAI-1) inhibits fibrinolysis and proteolysis. Basic fibroblast growth factor (bFGF) stimulates angiogenesis, which requires regional proteolysis. Because modulation of vasculopathy requires tight control of proteolysis, effects of bFGF on PAI-1 expression in endothelial cells (ECs) were characterized. bFGF increased PAI-1 mRNA and accumulation of PAI-1 protein in conditioned media in human umbilical vein ECs. The bFGF-mediated increase in PAI-1 mRNA was attenuated by inhibition of extracellular signal-regulated kinase kinase in human ECV304 cells. The rate of decrease in PAI-1 mRNA after actinomycin D treatment was not affected by bFGF. Transient transfection assays of the human PAI-1 promoter-luciferase construct demonstrated that bFGF-induced PAI-1 transcription was dependent on the elements within the -313 to -260 bp relative to the transcription start site. This region contains an E26 transformation specific 1 (Ets-1)-like site. Electrophoretic mobility shift assay showed that bFGF increased nuclear translocation or DNA binding of the Ets-1-like transcription factor to the PAI-1 promoter. Nucleotide substitution to disrupt the Ets-1-like site reduced bFGF-stimulated promoter activity. Fenofibric acid, an agonist ligand for the peroxisome proliferator-activated receptor-alpha, inhibited basal and bFGF-stimulated PAI-1 expression. By inducing PAI-1 expression from ECs, bFGF may control proteolysis and fibrinolysis in vessel walls.

UI MeSH Term Description Entries
D011345 Fenofibrate An antilipemic agent which reduces both CHOLESTEROL and TRIGLYCERIDES in the blood. Procetofen,Antara Micronized Procetofen,Apo-Feno-Micro,Apo-Fenofibrate,CiL,Controlip,Fenobeta,Fenofanton,Fenofibrat AL,Fenofibrat AZU,Fenofibrat AbZ,Fenofibrat FPh,Fenofibrat Heumann,Fenofibrat Hexal,Fenofibrat Stada,Fenofibrat-ratiopharm,Fénofibrate Debat,Fénofibrate MSD,Gen-Fenofibrate,LF-178,Lipanthyl,Lipantil,Liparison,Lipidil,Lipidil-Ter,Livesan,Lofibra,MTW-Fenofibrat,Normalip,Novo-Fenofibrate,Nu-Fenofibrate,PMS-Fenofibrate Micro,Phenofibrate,Procetofene,Secalip,Supralip,Tricor,durafenat,fenofibrat von ct,AZU, Fenofibrat,Apo Feno Micro,Apo Fenofibrate,Debat, Fénofibrate,Fenofibrat ratiopharm,Gen Fenofibrate,Heumann, Fenofibrat,Hexal, Fenofibrat,LF 178,LF178,Lipidil Ter,MTW Fenofibrat,Micronized Procetofen, Antara,Novo Fenofibrate,Nu Fenofibrate,PMS Fenofibrate Micro,Procetofen, Antara Micronized,Stada, Fenofibrat
D011500 Protein Synthesis Inhibitors Compounds which inhibit the synthesis of proteins. They are usually ANTI-BACTERIAL AGENTS or toxins. Mechanism of the action of inhibition includes the interruption of peptide-chain elongation, the blocking the A site of ribosomes, the misreading of the genetic code or the prevention of the attachment of oligosaccharide side chains to glycoproteins. Protein Synthesis Antagonist,Protein Synthesis Antagonists,Protein Synthesis Inhibitor,Antagonist, Protein Synthesis,Antagonists, Protein Synthesis,Inhibitor, Protein Synthesis,Inhibitors, Protein Synthesis,Synthesis Antagonist, Protein,Synthesis Inhibitor, Protein
D002460 Cell Line Established cell cultures that have the potential to propagate indefinitely. Cell Lines,Line, Cell,Lines, Cell
D003609 Dactinomycin A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015) Actinomycin,Actinomycin D,Meractinomycin,Cosmegen,Cosmegen Lyovac,Lyovac-Cosmegen,Lyovac Cosmegen,Lyovac, Cosmegen,LyovacCosmegen
D004247 DNA A deoxyribonucleotide polymer that is the primary genetic material of all cells. Eukaryotic and prokaryotic organisms normally contain DNA in a double-stranded state, yet several important biological processes transiently involve single-stranded regions. DNA, which consists of a polysugar-phosphate backbone possessing projections of purines (adenine and guanine) and pyrimidines (thymine and cytosine), forms a double helix that is held together by hydrogen bonds between these purines and pyrimidines (adenine to thymine and guanine to cytosine). DNA, Double-Stranded,Deoxyribonucleic Acid,ds-DNA,DNA, Double Stranded,Double-Stranded DNA,ds DNA
D004730 Endothelium, Vascular Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components. Capillary Endothelium,Vascular Endothelium,Capillary Endotheliums,Endothelium, Capillary,Endotheliums, Capillary,Endotheliums, Vascular,Vascular Endotheliums
D004791 Enzyme Inhibitors Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction. Enzyme Inhibitor,Inhibitor, Enzyme,Inhibitors, Enzyme
D005419 Flavonoids A group of phenyl benzopyrans named for having structures like FLAVONES. 2-Phenyl-Benzopyran,2-Phenyl-Chromene,Bioflavonoid,Bioflavonoids,Flavonoid,2-Phenyl-Benzopyrans,2-Phenyl-Chromenes,2 Phenyl Benzopyran,2 Phenyl Benzopyrans,2 Phenyl Chromene,2 Phenyl Chromenes
D006801 Humans Members of the species Homo sapiens. Homo sapiens,Man (Taxonomy),Human,Man, Modern,Modern Man
D000924 Anticholesteremic Agents Substances used to lower plasma CHOLESTEROL levels. Cholesterol Inhibitors,Hypocholesteremic Agents,Anticholesteremic Drugs,Anticholesteremics,Inhibitors, Cholesterol,Agents, Anticholesteremic,Agents, Hypocholesteremic,Drugs, Anticholesteremic

Related Publications

Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
January 1994, Life sciences,
Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
October 1996, Endocrinology,
Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
January 2009, Blood,
Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
November 1988, Cancer research,
Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
August 2002, Investigative ophthalmology & visual science,
Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
March 1995, Journal of cellular physiology,
Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
December 1991, Biochemical and biophysical research communications,
Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
June 1996, Blood coagulation & fibrinolysis : an international journal in haemostasis and thrombosis,
Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
November 1998, Journal of neurochemistry,
Takeaki Kaneko, and Satoshi Fujii, and Akio Matsumoto, and Daisuke Goto, and Naoki Ishimori, and Keiko Watano, and Tomoo Furumoto, and Taeko Sugawara, and Burton E Sobel, and Akira Kitabatake
March 1990, The Journal of cell biology,
Copied contents to your clipboard!