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Systemic tissue inhibitor of metalloproteinase‐1 gene delivery reduces neointimal hyperplasia in balloon‐injured rat carotid artery
Author(s) -
Furman C,
Luo Z,
Walsh K,
Duverger N,
Copin C,
Fruchart J.C,
Rouis M
Publication year - 2002
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/s0014-5793(02)03388-4
Subject(s) - restenosis , neointima , intimal hyperplasia , medicine , tissue inhibitor of metalloproteinase , tunica intima , neointimal hyperplasia , matrix metalloproteinase , systemic administration , artery , metalloproteinase , gene delivery , pathology , cardiology , genetic enhancement , carotid arteries , smooth muscle , stent , chemistry , biology , gene , biochemistry , microbiology and biotechnology , in vivo
Metalloproteinases (MMP)‐2 and MMP‐9 play a role in smooth muscle cell (SMC) migration from the media to the intima following arterial injury. Intravenous administration of adenovirus encoding tissue inhibitor of metalloproteinase‐1 (TIMP‐1) into balloon‐injured rat arteries (3×10 11 viral particles/rat; n =7) resulted in a transient expression of TIMP‐1 and a significant inhibition of neointima thickening within 16 days (∼40% vs. control; P =0.012). Three days after injury, the number of intimal SMCs was decreased by ∼98% in TIMP‐1‐treated rats. However, no alteration was seen in intimal SMC proliferation after 13 days of injury. Therefore, our results show that systemic gene transfer of TIMP‐1 is a promising approach in early restenosis treatment.