Hepatic stellate cells are an important cellular site for β-carotene conversion to retinoid

Hepatic stellate cells (HSCs) are responsible for storing 90–95% of the retinoid present in the liver. These cells have been reported in the literature also to accumulate dietary β-carotene, but the ability of HSCs to metabolize β-carotene in situ has not been explored. To gain understanding of this...

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Published in:Archives of biochemistry and biophysics 2010-12, Vol.504 (1), p.3-10
Main Authors: Shmarakov, Igor, Fleshman, Matthew K., D’Ambrosio, Diana N., Piantedosi, Roseann, Riedl, Ken M., Schwartz, Steven J., Curley, Robert W., von Lintig, Johannes, Rubin, Lewis P., Harrison, Earl H., Blaner, William S.
Format: Article
Language:English
Subjects:
Animals
beta Carotene - metabolism
beta-Carotene 15,15'-Monooxygenase - deficiency
beta-Carotene 15,15'-Monooxygenase - genetics
beta-Carotene 15,15'-Monooxygenase - metabolism
Carotene cleavage
Carotenoid
Chylomicron
Diet
Female
Gene Expression Regulation, Enzymologic
Hepatic Stellate Cells - metabolism
Hepatocytes - metabolism
Male
Mice
Retinoids - metabolism
RNA, Messenger - genetics
RNA, Messenger - metabolism
Vitamin A
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Summary:Hepatic stellate cells (HSCs) are responsible for storing 90–95% of the retinoid present in the liver. These cells have been reported in the literature also to accumulate dietary β-carotene, but the ability of HSCs to metabolize β-carotene in situ has not been explored. To gain understanding of this, we investigated whether β-carotene-15,15′-monooxygensase ( Bcmo1) and β-carotene-9′,10′-monooxygenase ( Bcmo2) are expressed in HSCs. Using primary HSCs and hepatocytes purified from wild type and Bcmo1-deficient mice, we establish that Bcmo1 is highly expressed in HSCs; whereas Bcmo2 is expressed primarily in hepatocytes. We also confirmed that HSCs are an important cellular site within the liver for accumulation of dietary β-carotene. Bcmo2 expression was found to be significantly elevated for livers and hepatocytes isolated from Bcmo1-deficient compared to wild type mice. This elevation in Bcmo2 expression was accompanied by a statistically significant increase in hepatic apo-12′-carotenal levels of Bcmo1-deficient mice. Although apo-10′-carotenal, like apo-12′-carotenal, was readily detectable in livers and serum from both wild type and Bcmo1-deficient mice, we were unable to detect either apo-8′- or apo-14′-carotenals in livers or serum from the two strains. We further observed that hepatic triglyceride levels were significantly elevated in livers of Bcmo1-deficient mice fed a β-carotene-containing diet compared to mice receiving no β-carotene. Collectively, our data establish that HSCs are an important cellular site for β-carotene accumulation and metabolism within the liver.
ISSN:0003-9861
1096-0384
DOI:10.1016/j.abb.2010.05.010