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J. Biol. Chem., Vol. 278, Issue 28, 25448-25453, July 11, 2003
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From the Division of Biopharmaceutics, Leiden Amsterdam Center for Drug Research, Gorlaeus Laboratories, Leiden University, P.O. Box 9502, Leiden, Zuid-Holland 2300 RA, The Netherlands
Hepatic cholesterol(ester) uptake from serum coupled to intracellular
processing and biliary excretion are important features in the removal of
excess cholesterol from the body. ATP-binding cassette (ABC) transporters play
an important role in hepatic cholesterol transport. The liver consists of
different cell types, and ABC transporters may exert different physiological
functions dependent on the individual cell type. Therefore, in the current
study, using real time PCR we compared the mRNA expression of ABC transporters
and genes involved in the regulation of cholesterol metabolism in liver
parenchymal, endothelial, and Kupffer cells. It appears that liver parenchymal
cells contain high expression levels compared with endothelial and Kupffer
cells of scavenger receptor class BI (
3-fold), peroxisome
proliferator-activated receptor (PPAR)
and PPAR
(8–20-fold), cholesterol 7-hydroxylase A1 (>100-fold), and
ABCG5/G8 (5-fold). Liver endothelial cells show a high expression of
cholesterol 27-hydroxylase, liver X receptor (LXR)
, PPAR
, and
ABCG1, suggesting a novel specific role for these genes in endothelial cells.
In Kupffer cells, the expression level of LXR, ABCA1, and in particular
ABCG1 is high, leading to an ABCG1 mRNA expression level that is 70-fold
higher than in parenchymal cells. It can be calculated that 51% of the total
liver ABCG1 expression resides in Kupffer cells and 24% in endothelial cells,
suggesting an intrahepatic-specific role for ABCG1 in Kupffer and endothelial
cells. Because of a specific stimulation of ABCG1 in parenchymal cells by a
high cholesterol diet, the contribution of parenchymal cells to the total
liver increased from 25 to 60%. Our data indicate that for studies of the role
of ABC transporters and their regulation in liver, their cellular localization
should be taken into account, allowing proper interpretation of metabolic
changes, which are directly related to their (intra)cellular expression
level.
Received for publication, February 4, 2003 , and in revised form, April 7, 2003.
* This work was supported by The Netherlands Organization for Scientific Research Grant 902-23-194. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Supported by Grant 2001 D041 from the Netherlands Heart Foundation.
To whom correspondence should be addressed. Tel.: 31-71-527-6238; Fax:
31-71-527-6032; E-mail:
Hoekstra{at}LACDR.Leidenuniv.nl.
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