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GTP cyclohydrolase I gene transfer reverses tetrahydrobiopterin deficiency and increases nitric oxide synthesis in endothelial cells and isolated vessels from diabetic rats.

Abstract:

Nitric oxide (NO) synthesis in endothelial cells is impaired in diabetes. We previously showed that impaired NO synthesis in the spontaneously diabetic BB (BBd) rat is due to decreased levels of tetrahydrobiopterin (BH4), secondary to decreased expression of GTP cyclohydrolase I (GTPCH). The aim of this study was to utilize adenoviral GTPCH gene transfer to reverse BH4 deficiency and repair the ability of endothelial cells to produce NO. GTPCH gene transfer increased BH4 levels in BBd endothe...

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Publication status:
Published

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Publisher copy:
10.1096/fj.04-1702fje

Authors


Meininger, CJ More by this author
Parker, JL More by this author
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Institution:
University of Oxford
Department:
Oxford, MSD, RDM, Cardiovascular Medicine, BHF Centre of Research Excellence
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Journal:
FASEB journal : official publication of the Federation of American Societies for Experimental Biology
Volume:
18
Issue:
15
Pages:
1900-1902
Publication date:
2004-12-05
DOI:
EISSN:
1530-6860
ISSN:
0892-6638
URN:
uuid:2803f535-8961-49a2-b299-b1babbba1379
Source identifiers:
105145
Local pid:
pubs:105145

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