@article{oai:az.repo.nii.ac.jp:00003927,
 author = {滝沢, 達也 and Takizawa, Tatsuya},
 journal = {麻布大学雑誌, Journal of Azabu University},
 month = {Mar},
 note = {生後3週齢のラット新生子の肝臓においてNO産生の亢進が認められ，このNO産生はeNOS Ser^1176のリン酸化により調節され，産生されたNOは肝細胞の増殖を維持していることが示唆された。, Hepatocytes have high ability to proliferate and are still undifferentiated in neonates. During development, the rat liver at 3 weeks after birth has been reported as the late maturation stage, increasing the number of the differentiated hepatocytes. Nitric oxide (NO) has been reported as a key mediator to enhance the hepatocyte proliferation in regenerating liver. However it is unclear that whether NO contributes to the hepatocyte proliferation in neonatal rat. We performed a semi-quantitative evaluation of endogenous NO production using a spin trap followed by electron paramagnetic resonance (EPR) spectroscopy with Fe-N, N-diethyldithiocarbamate (Fe-DETC) complex as a NO-trapping reagent in the rat liver during development. The NO production in the liver was increased at 3 weeks after birth and then declined. Administration of the NO synthase (NOS) inhibitor L-NAME suppressed the endogenous NO production and the hepatocyte proliferation in the rat liver at 3 weeks after birth. The phosphorylation level of NOS3 at Ser1177, the activating residue of the enzyme, was increased at 3 weeks after birth and then declined as well as the NO production pattern. These results suggest that NO is mainly synthesized by NOS3 up-regulated by phosphorylation at Ser1177 and enhances the hepatocyte proliferation in the rat liver at 3 weeks after birth. These findings provide a novel insight into the contribution of NO to hepatic growth and the liver maturation during development., P(論文), 40016759596, 特集, application/pdf, FEATURE ARTICLES},
 pages = {231--233},
 title = {肝臓におけるNO産生とその調節機構の解析},
 volume = {17/18},
 year = {2009}
}