ABCG5 and ABCG8 are expressed in gallbladder epithelial cells

Tauscher, Aimee; Kuver, Rahul

doi:10.1016/s0006-291x(03)01296-8

Cited by 44 publications

(45 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…1, lane 12). The anti-mouse Abcg5 antibody did not cross-react with dog Abcg5 which has been shown to be present in these cells [18]. Activity of the heterodimer on the plasmamembrane of the double transfected cells was also reflected in cholesterol efflux experiments.…”

Section: Resultsmentioning

confidence: 81%

“…DGBE mono transfected with Abcg5 or Abcg8 showed similar efflux as the non-transfected cells. The control efflux may be due to endogenous (dog) g5 and g8 [18]. Efflux was linear in time up to 120 min (data not shown).…”

Section: Resultsmentioning

confidence: 91%

“…Cells positive for GFP or DsRed or both were sorted using a Becton Dickinson FACS ARIA cell sorter. We chose gallbladder epithelial cells for the transfection because these cells grow polarized and express Abcg5 and g8 endogenously [18], hence accessory proteins required for transport of the heterodimer to the apical membrane are present.…”

Section: Construction and Production Of Lentiviral Vectorsmentioning

confidence: 99%

See 2 more Smart Citations

The sterol transporting heterodimer ABCG5/ABCG8 requires bile salts to mediate cholesterol efflux

et al. 2007

View full text Add to dashboard Cite

The ATP binding cassette transporters ABCG5 and ABCG8 are indispensable for hepatobiliary cholesterol transport. In this study, we investigated the specificity of the heterodimer for cholesterol acceptors. Dog gallbladder epithelial cells were mono-or double-transfected with lentiviral mouse Abcg5 and Abcg8 vectors. Double-transfected cells showed increased efflux to different bile salt (BS) species, while mono-transfected cells did not show enhanced efflux. The efflux was initiated at micellar concentrations and addition of phosphatidylcholine increased efflux. Cholesterol secretion was highly BS dependent, whereas other cholesterol acceptors such as ApoAI, HDL or methyl-b-cyclodextrin did not elicit Abcg5/g8 dependent cholesterol secretion.

show abstract

Section: Resultsmentioning

confidence: 81%

Section: Resultsmentioning

confidence: 91%

Section: Construction and Production Of Lentiviral Vectorsmentioning

confidence: 99%

See 1 more Smart Citation

The sterol transporting heterodimer ABCG5/ABCG8 requires bile salts to mediate cholesterol efflux

et al. 2007

View full text Add to dashboard Cite

show abstract

“…Both transporters are upregulated in gallbladders from patients with cholesterol gallstone disease [6]. Thus far, on the apical side the expression of ACBG5/G8 [7], scavenger receptor class B type I (SR-BI) [8], cubilin and megalin [9] was reported in gallbladder epithelial cells. The obligate heterodimer ABCG5/G8 is a cholesterol transporter expressed in enterocytes and hepatocytes, where it mediates the excretion of cholesterol and plant sterols out of the cell [1].…”

mentioning

confidence: 99%

The Neglected Cousin of the Hepatocyte: How Gallbladder Epithelial Cells Might Contribute to Cholesterol Gallstone Formation

Dikkers

Tietge

2013

Dig Dis Sci

View full text Add to dashboard Cite

“…23 Therefore, ABCG2 could work in concert with other half-transporters of the ABCG family implicated in sterol transport, namely ABCG5 and 8, which have recently been identified in gallbladder epithelium. 24 Moreover, ABCG2 can alter the organization of phospholipids in the plasma membrane, which in turn may influence cell surface properties and cellcell interactions. 25 The function of ABCG2 as an export pump for anticancer drugs and xenotoxins is consistent with a subcellular localization in the plasma membrane as demonstrated in normal and tumor cells as well as in various tumor cell lines.…”

mentioning

confidence: 99%

Subcellular localization of the ABCG2 transporter in normal and malignant human gallbladder epithelium

Aust

Obrist

Jaeger

et al. 2004

Laboratory Investigation

View full text Add to dashboard Cite

Epithelium of the gallbladder and biliary tract is exposed to high concentrations of potentially harmful exogenous and endogenous compounds excreted into primary bile. As the ATP-dependent efflux pump ABCG2 can prevent cellular accumulation of anticancer drugs, estrogen sulfate, xenobiotics, porphyrins, and sterols, its expression in the biliary tract might mediate protection by hindering their penetration. We therefore investigated the expression and subcellular distribution of ABCG2 in normal and malignant human gallbladder. After demonstrating ABCG2 expression in gallbladder epithelium by RT-PCR and Western blotting, we analyzed the subcellular localization of ABCG2 by indirect immunofluorescence in gallbladder adenocarcinoma specimens, and compared it to that in cholelithiasis, and normal gallbladder samples (n ¼ 54). In control, cholelithiasis, and well-differentiated tumor samples (grade 1, T1-3), ABCG2 is present at the luminal membrane of epithelial cells, which was proven by colocalization of apical-bound TRITC-labeled lectin (wheat germ agglutinin). In poorly differentiated gallbladder adenocarcinomas, intracellular ABCG2, in addition to luminal ABCG2 immunoreactivity, was found in 13/21 carcinoma samples (grade 2 and 3, T2-4, Po0.01). In 3/11 of grade 3 tumors, ABCG2 was present in the cytoplasmatic compartment only (Po0.01). In proliferating bile ducts of cholangiocarcinomas, ABCG2 showed an analogous staining pattern with presence in cytosolic compartments. However, the apical marker enzyme neutral endopeptidase remained on the membrane in all samples. To study whether phosphatidylinositol 3-kinase (PI3K) signaling might be necessary for ABCG2 membrane insertion, we treated freshly isolated human gallbladder epithelial cells with the PI3K inhibitor wortmannin. As assessed by indirect immunofluorescence, this maneuver redistributes ABCG2 to intracellular compartments. In conclusion, our data suggest a protective role for ABCG2 in well-differentiated gallbladder epithelial cells. Cytoplasmatic accumulation of ABCG2 in poorly differentiated carcinomas might coincide with malfunctioning of PI3K-signaling pathways during tumor progression. Laboratory Investigation (2004) 84, 1024-1036, advance online publication, 7 May 2004; doi:10.1038/labinvest.3700127Keywords: ABCG2; gallbladder epithelium; gallbladder carcinoma; cholelithiasis; phosphatidylinositol 3-kinase; BCRP; neutral endopeptidase Cholelithiasis, and as a complication, acute cholecystitis, are among the most common gastrointestinal diseases in industrialized countries, while carcinomas of the gallbladder are quite rare. Although cholelithiasis is considered an important risk factor for gallbladder carcinoma, only 1-2% of patients who have operations for gallstones are diagnosed with gallbladder cancer at the time of surgery. The epidemiological characteristics of cholelithiasis and gallbladder cancer are closely related. Risk factors associated with the formation of cholesterol gallstones including estrogen exposure, nutritional factors, obesity...

show abstract

ABCG5 and ABCG8 are expressed in gallbladder epithelial cells

Cited by 44 publications

References 29 publications

The sterol transporting heterodimer ABCG5/ABCG8 requires bile salts to mediate cholesterol efflux

The sterol transporting heterodimer ABCG5/ABCG8 requires bile salts to mediate cholesterol efflux

The Neglected Cousin of the Hepatocyte: How Gallbladder Epithelial Cells Might Contribute to Cholesterol Gallstone Formation

Subcellular localization of the ABCG2 transporter in normal and malignant human gallbladder epithelium

Contact Info

Product

Resources

About