Gene Therapy for Vascular Smooth Muscle Cell Proliferation After Arterial Injury
Accumulation of vascular smooth muscle cells as a consequence of arterial injury is a major feature of vascular proliferative disorders. Molecular approaches to the inhibition of smooth muscle cell proliferation in these settings could potentially limit intimal expansion. This problem was approached...
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| Published in: | Science (American Association for the Advancement of Science) Vol. 265; no. 5173; pp. 781 - 784 |
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| Main Authors: | , , , , , , |
| Format: | Journal Article |
| Language: | English |
| Published: |
United States
American Society for the Advancement of Science
05.08.1994
American Association for the Advancement of Science |
| Subjects: | |
| ISSN: | 0036-8075, 1095-9203 |
| Online Access: | Get full text |
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| Abstract | Accumulation of vascular smooth muscle cells as a consequence of arterial injury is a major feature of vascular proliferative disorders. Molecular approaches to the inhibition of smooth muscle cell proliferation in these settings could potentially limit intimal expansion. This problem was approached by introducing adenoviral vectors encoding the herpesvirus thymidine kinase (tk) into porcine arteries that had been injured by a balloon on a catheter. These smooth muscle cells were shown to be infectable with adenoviral vectors, and introduction of the tk gene rendered them sensitive to the nucleoside analog ganciclovir. When this vector was introduced into porcine arteries immediately after a balloon injury, intimal hyperplasia decreased after a course of ganciclovir treatment. No major local or systemic toxicities were observed. These data suggest that transient expression of an enzyme that catalyzes the formation of a cytotoxic drug locally may limit smooth muscle cell proliferation in response to balloon injury. |
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| AbstractList | Accumulation of vascular smooth muscle cells as a consequence of arterial injury is a major feature of vascular proliferative disorders. Molecular approaches to the inhibition of smooth muscle cell proliferation in these settings could potentially limit intimal expansion. This problem was approached by introducing adenoviral vectors encoding the herpesvirus thymidine kinase (tk) into porcine arteries that had been injured by a balloon on a catheter. These smooth muscle cells were shown to be infectable with adenoviral vectors, and introduction of the tk gene rendered them sensitive to the nucleoside analog ganciclovir. When this vector was introduced into porcine arteries immediately after a balloon injury, intimal hyperplasia decreased after a course of ganciclovir treatment. No major local or systemic toxicities were observed. These data suggest that transient expression of an enzyme that catalyzes the formation of a cytotoxic drug locally may limit smooth muscle cell proliferation in response to balloon injury. Accumulation of vascular smooth muscle cells as a consequence of arterial injury is a major feature of vascular proliferative disorders. Molecular approaches to the inhibition of smooth muscle cell proliferation in these settings could potentially limit intimal expansion. This problem was approached by introducing adenoviral vectors encoding the herpesvirus thymidine kinase (tk) into porcine arteries that had been injured by a balloon on a catheter. These smooth muscle cells were shown to be infectable with adenoviral vectors, and introduction of the tk gene rendered them sensitive to the nucleoside analog ganciclovir. When this vector was introduced into porcine arteries immediately after a balloon injury, intimal hyperplasia decreased after a course of ganciclovir treatment. No major local or systemic toxicities were observed. These data suggest that transient expression of an enzyme that catalyzes the formation of a cytotoxic drug locally may limit smooth muscle cell proliferation in response to balloon injury.Accumulation of vascular smooth muscle cells as a consequence of arterial injury is a major feature of vascular proliferative disorders. Molecular approaches to the inhibition of smooth muscle cell proliferation in these settings could potentially limit intimal expansion. This problem was approached by introducing adenoviral vectors encoding the herpesvirus thymidine kinase (tk) into porcine arteries that had been injured by a balloon on a catheter. These smooth muscle cells were shown to be infectable with adenoviral vectors, and introduction of the tk gene rendered them sensitive to the nucleoside analog ganciclovir. When this vector was introduced into porcine arteries immediately after a balloon injury, intimal hyperplasia decreased after a course of ganciclovir treatment. No major local or systemic toxicities were observed. These data suggest that transient expression of an enzyme that catalyzes the formation of a cytotoxic drug locally may limit smooth muscle cell proliferation in response to balloon injury. |
| Audience | Academic |
| Author | Imperiale, Michael J. Ohno, Takeshi Gordon, David Pompili, Vincent J. San, Hong Nabel, Gary J. Nabel, Elizabeth G. |
| Author_xml | – sequence: 1 givenname: Takeshi surname: Ohno fullname: Ohno, Takeshi – sequence: 2 givenname: David surname: Gordon fullname: Gordon, David – sequence: 3 givenname: Hong surname: San fullname: San, Hong – sequence: 4 givenname: Vincent J. surname: Pompili fullname: Pompili, Vincent J. – sequence: 5 givenname: Michael J. surname: Imperiale fullname: Imperiale, Michael J. – sequence: 6 givenname: Gary J. surname: Nabel fullname: Nabel, Gary J. – sequence: 7 givenname: Elizabeth G. surname: Nabel fullname: Nabel, Elizabeth G. |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/8047883$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright 1994 American Association for the Advancement Science COPYRIGHT 1994 American Association for the Advancement of Science COPYRIGHT 1994 American Association for the Advancement of Science |
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| Title | Gene Therapy for Vascular Smooth Muscle Cell Proliferation After Arterial Injury |
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