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Expression of scavenger receptor class B type I in gallbladder columnar epithelium.

Journal article
Authors Magnus S.C. Johnson
Per-Arne Svensson
Jan Borén
Håkan Billig
Lena M S Carlsson
Björn Carlsson
Published in Journal of gastroenterology and hepatology
Volume 17
Issue 6
Pages 713-20
ISSN 0815-9319
Publication year 2002
Published at Institute of Physiology and Pharmacology, Dept of Physiology
Pages 713-20
Language en
Keywords Animals, Antigens, CD36, metabolism, Apolipoprotein B-100, Apolipoproteins B, metabolism, Blotting, Western, Cholesterol, LDL, blood, Cholesterol, VLDL, blood, Epithelium, metabolism, Gallbladder, metabolism, Immunohistochemistry, Membrane Proteins, Mice, Mice, Transgenic, Receptors, Immunologic, Receptors, Lipoprotein, Receptors, Scavenger, Reverse Transcriptase Polymerase Chain Reaction, Scavenger Receptors, Class B
Subject categories Basic Medicine


The lipid content of bile may be modified by the gallbladder epithelium. Recent studies indicate that cholesterol can be absorbed from bile and that this can be enhanced by apolipoprotein (apo) A-I. SR-BI is a multifunctional receptor capable of binding a wide array of native or modified lipoproteins, phospholipid or bile acid micelles. As apo A-I is a ligand for scavenger receptor class B type I (SR-BI) we have characterized the expression of this receptor in murine gallbladder.Reverse transcription-polymerase chain reaction (RT-PCR), immunoblotting and immunohistochemistry were used to study SR-BI expression in murine gallbladders. SR-BI expression was also used to examine gallbladders from high-fat-fed wild-type and apo B-100 transgenic mice.SR-BI and SR-BII mRNA are expressed in gallbladder. SR-BI immunoreactivity was localized to the columnar epithelium of the gallbladder. Immunoreactive SR-BI in gallbladder had an estimated molecular weight of 57 kDa, in contrast to the expected 82 kDa. Deglycosylation experiments indicated that the size difference between the two forms of the receptor is due to post-translational modification. Fat feeding of apo B transgenic mice resulted in gallstone formation but had no effect on the abundance of SR-BI.Gallbladder epithelial cells express SR-BI. This opens the possibility that SR-BI may influence the modification of bile in the gallbladder.

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