The DOI matches its Crossref record; 32 of the 32 references it cites were found in a registry or an index.
Role of the arginine-nitric oxide pathway in the regulation of vascular smooth muscle cell proliferation
Open accessAbstract
The objective of this study was to elucidate the mechanisms by which nitric oxide (NO) inhibits rat aortic smooth muscle cell (RASMC) proliferation. Two products of the arginine-NO pathway interfere with cell growth by distinct mechanisms. N G -hydroxyarginine and NO appear to interfere with cell proliferation by inhibiting arginase and ornithine decarboxylase (ODC), respectively. S -nitroso- N -acetylpenicillamine, ( Z )-1-[ N -(2-aminoethyl)- N -(2-aminoethyl)-amino]-diazen-1-ium-1,2-diolate, and a nitroaspirin derivative (NCX 4016), each of which is a NO donor agent, inhibited RASMC growth at concentrations of 1–3 μM by cGMP-independent mechanisms. The cytostatic action of the NO donor agents as well as α-difluoromethylornithine (DFMO), a known ODC inhibitor, was prevented by addition of putrescine but not ornithine. These observations suggested that NO, like DFMO, may directly inhibit ODC. Experiments with purified, recombinant mammalian ODC revealed that NO inhibits ODC possibly by S-nitrosylation of the active site cysteine in ODC. DFMO, as well as the NO donor agents, interfered with cellular polyamine (putrescine, spermidine, spermine) production. Conversely, increasing the expression and catalytic activity of arginase I in RASMC either by transfection of cells with the arginase I gene or by induction of arginase I mRNA with IL-4 resulted in increased urea and polyamine production as well as cell proliferation. Finally, coculture of rat aortic endothelial cells, which had been pretreated with lipopolysaccharide plus a cytokine mixture to induce NO synthase and promote NO production, caused NO-dependent inhibition of target RASMC proliferation. This study confirms the inhibitory role of the arginine-NO pathway in vascular smooth muscle proliferation and indicates that one mechanism of action of NO is cGMP-independent and attributed to its capacity to inhibit ODC.
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Regulatory role for the arginine–nitric oxide pathway in metabolism of energy substrates
Jobgen, W. S., Fried, S. K., Fu, W. J., Meininger, C. J., & Wu, G. (2006) · The Journal of Nutritional Biochemistry · doi:10.1016/j.jnutbio.2005.12.001 · Cited by 710
Self-citationARGINASE: A CRITICAL REGULATOR OF NITRIC OXIDE SYNTHESIS AND VASCULAR FUNCTION
Durante, W., Johnson, F. K., & Johnson, R. A. (2007) · Clinical and Experimental Pharmacology and Physiology · doi:10.1111/j.1440-1681.2007.04638.x · Cited by 577
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Modulation of Prostaglandin Biosynthesis by Nitric Oxide and Nitric Oxide Donors
Mollace, V., Muscoli, C., Masini, E., Cuzzocrea, S., & Salvemini, D. (2005) · Pharmacological Reviews · doi:10.1124/pr.57.2.1 · Cited by 357
Metadata
- Authors
- Ignarro, L. J., Buga, G. M., Wei, L. H., Bauer, P. M., Wu, G., & del Soldato, P.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2001-03-20
- Volume
- 98
- Issue
- 7
- Pages
- 4202-4208
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2133040336
- Cited by
- 331
- References
- 32
- FWCI
- 13.26
- Type
- journal article
- Language
- en
- Open access
- green
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