Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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Hirano, K. et al.

Hirano, Ikegami, Tsujii, Zhang, Matsuura, Nakagawa-Toyama, Koseki, Masuda, Maruyama, Shimomura, Ueda, Yamashita,

Probucol enhances the expression of human hepatic scavenger receptor class B type I, possibly through a species-specific mechanism.

OBJECTIVE: Scavenger receptor class B type I ( SR-BI) is a major receptor for high-density lipoproteins (HDL) in the liver, which is the terminus of reverse cholesterol transport. Overexpression of SR-BI attenuated experimental atherosclerosis in murine models, concomitant with a reduction in plasma HDL-cholesterol levels. Probucol is known to be a potent hypolipidemic drug to regress xanthoma formation and carotid atherosclerosis in conjunction with a marked reduction in HDL-cholesterol levels. The aim of the present study was to know the effect of probucol on the expression of SR-BI and the underlying mechanism. METHODS AND RESULTS: We found that probucol increased the expression of SR-BI proteins in in vitro human liver cells and an in vivo rabbit model, but not in wild-type C57Bl6 mice. The decay curve of SR-BI protein was markedly retarded in probucol-treated HepG2 cells in the presence of cycloheximide, indicating that probucol may stabilize human SR-BI protein. To determine the underlying mechanism for the observed species-specific effect, we conducted the following host-swap experiments, in which SR-BI was transfected or expressed in heterologous cells or hosts. Probucol did not increase human SR-BI protein in the liver of transgenic mice carrying the entire human SR-BI genome. Although probucol could stabilize even murine SR-BI, when transfected into a human cell line, HepG2, human SR-BI was not stabilized in a mouse hepatoma cell line, Hepa 1-6, treated with probucol. CONCLUSIONS: Probucol enhances hepatic SR-BI protein expression, possibly through species-specific stabilization of the protein.[1]

References

Probucol enhances the expression of human hepatic scavenger receptor class B type I, possibly through a species-specific mechanism. Hirano, K., Ikegami, C., Tsujii, K., Zhang, Z., Matsuura, F., Nakagawa-Toyama, Y., Koseki, M., Masuda, D., Maruyama, T., Shimomura, I., Ueda, Y., Yamashita, S. Arterioscler. Thromb. Vasc. Biol. (2005) [Pubmed]

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