Endothelium-targeted transgenic GTP-cyclohydrolase I overexpression inhibits neointima formation in mouse carotid artery.

Journal article

1. Tetrahydrobiopterin (BH(4)) is an essential cofactor that maintains the normal function of endothelial nitric oxide (NO) synthase. Restenosis is a key complication after transluminal angioplasty. Guanosine 5'-triphosphate-cyclohydrolase I (GTPCH) is the first rate-limiting enzyme for de novo BH(4) synthesis. However, the role of GTPCH in restenosis is not fully understood. The present study tested the hypothesis that endothelial-targeted GTPCH overexpression retards neointimal formation, a...

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Authors: Liao, S; Lin, L; Zeng, J; Huang, R; Channon, K

• Publication status: Published
• Journal: Clinical and experimental pharmacology and physiology
• Volume: 34
• Issue: 12
• Pages: 1260-1266
• Publication date: 2007-12-01
• DOI: 10.1111/j.1440-1681.2007.04719.x
• EISSN: 1440-1681
• ISSN: 0305-1870
• Language: English
• Keywords: Aorta; Hypertrophy; Coronary Restenosis; Mice, Transgenic; Animals; Mice, Inbred C57BL; Male; Tunica Intima; GTP Cyclohydrolase; Biopterin; Mice; Carotid Arteries; Nitric Oxide