DNA antisense strategies in the study of receptors for vasoactive peptides, and of growth and wound-healing factors

DNA antisense strategies in the study of receptors for vasoactive peptides, and of growth and wound-healing factors

Autor DOrleansJuste, P. Google Scholar
Sirois, M. G. Google Scholar
Edelman, E. R. Google Scholar
Regoli, D. Google Scholar
Pheng, L. H. Google Scholar
Bkaily, G. Google Scholar
Lindsey, C. J. Google Scholar
Instituição UNIV SHERBROOKE
HARVARD UNIV
Universidade Federal de São Paulo (UNIFESP)
Resumo Antisense oligodeoxynucleotide technology has contributed greatly to the overall understanding of both mRNA stability as well as translational processes leading to protein synthesis. Arrest of translational processes by DNA antisense strands usually reduces maximal effects of agonists without affecting their apparent affinities in treated isolated vascular or nonvascular preparations.In the present study, examples are given of DNA antisense oligonucleotide-induced repression of receptors for endothelins, kinins as well as of the platelet-derived growth factor. Furthermore, the efficiency of this technology illustrates the roles of protooncogenes (c-myc and c-myb) in wound-healing mechanisms.The overall mechanism of action of these oligomers is described and the relevance of size, chemical alterations and mode of delivery are illustrated. Release of oligophosphorothioates from polymer matrices and gels can produce a prolonged effect in vivo. Antisense oligonucleotides remain essential in experimental models for which receptor antagonists or selective inhibitors of intracellular components are currently unavailable.
Palavra-chave DNA antisense
oligophosphodiester
oligophosphorothioate
ETA and B-1 receptors
c-myc and c-myb protooncogenes
PDGF-beta receptor subunit
Idioma Inglês
Data de publicação 1997-07-01
Publicado em Molecular and Cellular Biochemistry. Dordrecht: Kluwer Academic Publ, v. 172, n. 1-2, p. 199-211, 1997.
ISSN 0300-8177 (Sherpa/Romeo, fator de impacto)
Publicador Kluwer Academic Publ
Extensão 199-211
Fonte http://dx.doi.org/10.1023/A:1006800629012
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:A1997XU44700021
Endereço permanente http://repositorio.unifesp.br/handle/11600/25759

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