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Research Article Free access | 10.1172/JCI117070
Cancer Research Center, La Jolla Cancer Research Foundation, California 92037.
Find articles by Wolf, Y. in: JCI | PubMed | Google Scholar
Cancer Research Center, La Jolla Cancer Research Foundation, California 92037.
Find articles by Rasmussen, L. in: JCI | PubMed | Google Scholar
Cancer Research Center, La Jolla Cancer Research Foundation, California 92037.
Find articles by Ruoslahti, E. in: JCI | PubMed | Google Scholar
Published March 1, 1994 - More info
Intimal hyperplasia is induced by therapeutic vascular interventions and often results in clinically important narrowing of the vascular lumen. Examination of the role of TGF-beta 1 in a rat carotid artery injury model confirmed the presence of a previously reported increase in TGF-beta 1 mRNA in the media of injured arteries. Administration of neutralizing anti- TGF-beta 1 antibodies significantly (P < 0.05) reduced the size of the intimal lesions that developed after carotid balloon injury. A control antibody had no effect. The intimal/medial area ratio was also reduced in the anti-TGF-beta 1 group relative to controls (P < 0.01). Immunohistochemical staining showed that two TGF-beta 1-induced extracellular matrix components, EDA + fibronectin and versican, were greatly increased in the untreated neointimal lesions, but were almost completely absent from the lesions of the anti-TGF-beta 1-treated animals. We conclude that TGF-beta 1 is causally involved in the development of intimal hyperplasia, and that anti-TGF-beta 1 agents may be useful in achieving at least partial control of this condition.
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