Use of RNA interference to inhibit integrin subunit alphaV-mediated angiogenesis.

One of the central molecules in capillary formation during angiogenesis is the integrin alphaVbeta3. The aim of this study was to inhibit alphaV-mediated angiogenesis in vitro using RNAs (siRNA) as well as antisense oligodeoxyribonucleotides (asON). Five siRNAs, against the alphaV chain of alphaVbeta3, and three asON, which had the respective sequence of the antisense sequence of three of the siRNAs molecules, were examined.

Advantages of antisense drugs for the treatment of oral diseases.

For almost two decades, antisense oligonucleotides (AS-ON) have been used successfully to suppress and regulate gene expression in vitro and in vivo. They are, meanwhile, well established to serve as molecular tools for several biologic applications, from the study of single gene functions up to complex target gene validations. Based on an at least theoretically simple mode of action, the sequence-specific inhibition of mRNA functions after complex formation by Watson-Crick base pairing and presumably enzymatic degradation of the target mRNA, they obviously carry a high therapeutic potential for the treatment of human diseases.

Inhibition of angiogenesis in vitro by alphav integrin-directed antisense oligonucleotides.

The integrin alpha v beta 3 plays a central role in angiogenesis. In this study, we used antisense oligodeoxyribonucleotides (ONs) directed against the alpha v subunit of alpha v beta 3 to inhibit integrin expression. Ten ON sequences, which were selected by systematic alignment of computer-predicted secondary structures of alpha v mRNA, were transfected into human umbilical vein endothelial cells (HUVECs).

Antisense-mediated inhibition of ICAM-1 expression: a therapeutic strategy against inflammation of human periodontal tissue.

Periodontal diseases, such as gingivitis and periodontitis, are caused by a mixed infection by several types of bacteria in the dental plaque, causing a chronic inflammation of the gingival mucosa. Inflammatory processes in conjunction with immune responses to bacterial attacks are generally protective. In profound periodontitis, however, hyperresponsiveness and hypersensitivity of the immune system are counterproductive because of the destruction of the affected periodontal connective tissues.