Effects of trapidil (triazolopyrimidine), a platelet-derived growth factor antagonist, in preventing restenosis after percutaneous transluminal coronary angioplasty

Okamoto, Shinya; Inden, M; Setsuda, Morimichi; Konishi, Tokuji; Nakano, Takeshi

doi:10.1016/0002-8703(92)90792-t

Cited by 88 publications

(51 citation statements)

References 10 publications

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“…Antibodies to PDGF can inhibit the formation of neointima in injured arteries in rats (19), and an inhibitor of PDGF, trapadil, may limit restenosis in humans (62). Since neointima formation and restenosis after angioplasty are thought to be primarily a consequence of smooth muscle cell proliferation and migration, this provides further evidence for the role of PDGF in generating large vessels.…”

Section: Skin Flapmentioning

confidence: 96%

Platelet-derived growth factor BB induces functional vascular anastomoses in vivo.

Brown

Hong

Farrell

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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Section: Skin Flapmentioning

confidence: 96%

Platelet-derived growth factor BB induces functional vascular anastomoses in vivo.

Brown

Hong

Farrell

et al. 1995

Proc. Natl. Acad. Sci. U.S.A.

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“…Agents that prevent the stimulation of SMC by growth factors, such as trapidil (an antiplatelet drug that also antagonists PDGF [214]) minimise proliferation and migration in animal studies, whether delivered systemically [214,215] or locally [216]. Trapidil can also reduce the rate of clinical restenosis [10,39,217]. Locally delivered antisense TGF-β 1 , has been administered to arteries via pluronic gels applied to the arterial adventitia, and to vein grafts using nanoparticles, with a subsequent reduction in neointimal thickening [116,218].…”

Section: Antiproliferative and Antimigrating Agentsmentioning

confidence: 99%

Targeted Treatments for Restenosis and Vein Graft Disease

Thomas

2012

ISRN Vascular Medicine

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Surgery to restore blood flow in arteries blocked by atherosclerotic plaque is a common treatment in cardiovascular disease. Longterm complications of surgical treatment are vein graft disease and restenosis, a renarrowing of the blood vessel after bypass or removal of the culprit atherosclerotic plaque. Attempts to prevent or treat these complications by systemic pharmacological approaches have been largely unsuccessful in the clinic. This has led to an interest in developing targeted or locally delivered strategies. This paper discusses many of the various site-delivered therapies that are under examination as potential antirestenotic and antivein graft disease agents (including antithrombotic, antiproliferative, and anti-inflammatory agents) and why many therapies developed in animal models fail in clinical trials. Techniques of targeted delivery (including stents, "magic bullets," and adventitial delivery) and delivery systems (including nanoparticles and the use of gene therapy) are also discussed.

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“…The MMR system recognizes and repairs mispaired or unpaired nucleotides that result from errors in DNA replication (32,33). The mammalian homologues of the E. Coli MutS protein form heterodimers (MSH2-MSH6 and MSH2-MSH3) that bind to nucleotide mismatches and recruit heterodimers of the MutL homologues (MLH1-PMS2, MLH1-PMS1, or MLH1-MLH3) to base mismatches (32,34).…”

Section: Bodymentioning

confidence: 99%

“…Co-morbidity factors such as dietary iron, estrogen and endotoxin appear to be needed (31)(32)(33)(34).…”

Section: /09/00 Pagementioning

confidence: 99%

Bone-97 Alcohol and Skeletal Adaptation to Mechanical Usage

Turner¹

2002

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Public reporting burden for this collection of information Is estimated to average 1 hour per response, including the time for reviewing instructions, searching existing data sources, gathering and maintaining the data needed, and completing and reviewing this collection of Information. Send comments regarding this burden estimate or any other aspect of this collection of information, including suggestions for reducdng this burden to Washington Headquarters Services, Directorate for Intforation Operations and Reports, 1215 Jefferson Davis Highway, Suite 1204, Adington, VA 22202-4302, and to the Office of Management and Budget, AUTHOR(S)Vincent L. Cryns, M.D. PERFORMING ORGANIZATION NAME(S) AND ADDRESS(ES) 8. PERFORMING ORGANIZATION REPORT NUMBERNorthwestern University Chicago, Illinois 60611 E-Mall:v-cryns@northwestern.edu SPONSORING I MONITORING AGENCY NAME(S) AND ADDRESS(ES)10. SPONSORING / MONITORING AGENCY REPORT NUMBER U.S. Army Medical Research and Materiel CommandFort Detrick, Maryland 21702-5012 SUPPLEMENTARY NOTES Original contains color plates:All DTIC reproductions will be in black and white. Abstract (Maximum 200 Words) (abstract should contain no proprietary or confidential information)Using a novel expression cloning strategy and secondary functional screen of a human prostate cancer cDNA library, we have identified one new, functionally relevant caspase substrate: the mismatch repair protein MLHI implicated in a variety of cancers including those of the prostate. We have demonstrated that human MLH1 is specifically cleaved by caspase-3 (but not by other caspases) at ASP418 in vitro. Furthermore, we have shown that MLH1 is rapidly proteolyzed by caspase-3 in prostate cancer cells induced to undergo apoptosis by treatment with TNF-related apoptotosis-inducing ligand (TRAIL) or the topoisomerase II inhibitor etoposide, which induces DNA double-strand breaks. Importantly, proteolysis of MLH1 by caspase-3 triggers its partial redistribution from the nucleus to the cytoplasm. In addition, a capase-3 cleavage-resistant D418E MLHII mutant inhibits etoposide-induced apoptosis but has little effect on TRAIL-induced apoptosis. These results indicate that MLHI is specifically targeted for proteolysis by caspase-3, and this proteolytic event promotes the execution of apoptotic signals initiated by DNA double-strand breaks. In this way, our results suggest a novel function of MLHI in the response to DNA double-strand breaks that is deregulated by caspase proteolysis. These experiments, then, may lead to novel treatments for prostate cancer that specifically target MLH1. IntroductionApoptosis or programmed cell death is a genetically regulated cellular suicide response that is activated in prostate cancer cells by androgen ablation and irradiation. Indeed, the tumoricidal activity of these treatment modalities stems from their ability to induce apoptosis in prostate cancer cells (1). Caspases are a conserved family of cysteine proteases that are universal effectors of programmed cell death (2, 3). However, t...

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Effects of trapidil (triazolopyrimidine), a platelet-derived growth factor antagonist, in preventing restenosis after percutaneous transluminal coronary angioplasty

Cited by 88 publications

References 10 publications

Platelet-derived growth factor BB induces functional vascular anastomoses in vivo.

Platelet-derived growth factor BB induces functional vascular anastomoses in vivo.

Targeted Treatments for Restenosis and Vein Graft Disease

Bone-97 Alcohol and Skeletal Adaptation to Mechanical Usage

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