Carcinoembryonic antigen-related cell adhesion molecule 1 is the 85-kilodalton pronase-resistant biliary glycoprotein in the cholesterol crystallization promoting low density protein-lipid complex

Jirsa, M; Muchová, Lucie; Dráberová, Lubica; Dráber, Petr; Šmíd, F.; Kuroki, Masahide; Marecek, Z; Groen, Albert K.

doi:10.1053/jhep.2001.29372

Cited by 9 publications

(5 citation statements)

References 34 publications

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“…We have also observed a moderate repression of carcinoembryonic antigen‐related cell adhesion molecule 9 (CEACAM9). Members of the CEACAM family of proteins play a role in the biliary cholesterol crystallization, promoting low‐density protein–lipid complex [31], and serve as a potent angiogenic factor and a major effector of vascular endothelial growth factor [32]. These data suggest that dietary cholesterol reduces cardiac cholesterol synthesis and transport, and confirm our previous assumptions that high‐cholesterol diet inhibits the mevalonate pathway thereby reducing protein prenylation and ubiquinone synthesis [9].…”

Section: Resultssupporting

confidence: 85%

Cholesterol diet‐induced hyperlipidemia influences gene expression pattern of rat hearts: a DNA microarray study

et al. 2004

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To pro¢le gene expression patterns involved in the direct myocardial e¡ect of cholesterol-enriched diet-induced hyperlipidemia, we monitored global gene expression changes by DNA microarray analysis of 3200 genes in rat hearts. Twentysix genes exhibited signi¢cant up-regulation and 25 showed down-regulation in hearts of rats fed a 2% cholesterol-enriched diet for 8 weeks as compared to age-matched controls. The expression changes of 12 selected genes were also assessed by real-time quantitative polymerase chain reaction. Genes with altered expression in the heart due to hyperlipidemia included procollagen type III, co¢lin/destrin, tensin, transcription repressor p66, synaptic vesicle protein 2B, Hsp86, chaperonin subunit 5O O, metallothionein, glutathione S-transferase, protein kinase C inhibitor, ATP synthase subunit c, creatine kinase, chloride intracellular channel 4, NADH oxidoreductase and dehydrogenase, ¢bronectin receptor L L chain, CD81 antigen, farnesyltransferase, calreticulin, disintegrin, p120 catenin, Smad7, etc. Although some of these genes have been suspected to be related to cardiovascular diseases, none of the genes has been previously shown to be involved in the mechanism of the cardiac e¡ect of hyperlipidemia.

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Section: Resultssupporting

confidence: 85%

Cholesterol diet‐induced hyperlipidemia influences gene expression pattern of rat hearts: a DNA microarray study

et al. 2004

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“…S5 ). It should be noted that the immunoblot for CEACAM1 in the CD36 IP resulted in the detection of bands at 130 and 85 kDa, the former corresponding to the expected molecular mass of CEACAM1-LF, and the latter to the molecular mass of BGP1 ( 4 ). Given the lower molecular mass of BGP1 versus CEACAM1, it is likely that BGP1 is a proteolytic fragment of CEACAM1.…”

Section: Resultsmentioning

confidence: 99%

“…This relationship suggests the possibility that the steady-state levels of lipid droplets depend on BC function. Since it is well known that reverse cholesterol transport from the liver to intestine occurs through bile ( 75 ), and that BGP1 is a major cholesterol associated component of bile ( 4 , 76 ), it would not be a surprise if hepatocytes also had the capacity to reverse transport other lipids into bile. Indeed, phospholipids constitute a major portion (10–20 mol percent) of bile ( 47 ).…”

Section: Discussionmentioning

confidence: 99%

“…BGP1, now known as CEACAM1 ( 2 ), is highly expressed on the membranes of hepatocytes and bile canaliculi (BC), and as a coreceptor of insulin receptor, is responsible for insulin clearance in portal circulation ( 3 ). Since CEACAM1 binds to cholesterol in bile ( 4 ), is highly expressed in the intestinal tract ( 5 ), and is a homotypic cell adhesion molecule, it is likely that CEACAM1 plays a more general role in lipid homeostasis, from lipid uptake in the intestine to storage in the liver. Signaling of the cytoplasmic domain isoforms of CEACAM1-SF (short form, 12 amino acids) or CEACAM1-LF (long form, 72 amino acids) has been studied in epithelial cells ( 6 ), lymphocytes ( 7 ), endothelial cells ( 8 ), and hepatocytes ( 3 ).…”

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confidence: 99%

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Human CEACAM1-LF regulates lipid storage in HepG2 cells via fatty acid transporter CD36

Chean

Chen

Gugiu

et al. 2021

Journal of Biological Chemistry

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This is a PDF file of an article that has undergone enhancements after acceptance, such as the addition of a cover page and metadata, and formatting for readability, but it is not yet the definitive version of record. This version will undergo additional copyediting, typesetting and review before it is published in its final form, but we are providing this version to give early visibility of the article. Please note that, during the production process, errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.

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“…Factors affecting cholesterol crystal nucleation are studied for bile proteins and non-protein components in the past years [37]. Studies comparing cholesterol gallstone-containing biles have provided unique information on lectin-binding glycoproteins [38,39], and further information is needed to clarify their significance in the cholesterol pathogenesis.…”

Section: Prolonged Intestinal Transitionmentioning

confidence: 99%

Recent understanding of cholesterol gallstone pathogenesis: implication to non-surgical therapeutic strategy

Tazuma

2008

Clin J Gastroenterol

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This article reviews the recent understanding of cholesterol gallstone pathogenesis in light of etiology and molecular mechanisms of the cholesterol gallstone formation process, to provide the future direction of a non-surgical therapeutic strategy. In principle, cholesterol gallstone formation, which is associated with an altered bile salt metabolism, is based primarily upon the impairment of cholesterol metabolism and homeostasis. Cholesterol is eliminated physiologically into bile; thus, the excess cholesterol induces bile metastability due to a relative insufficiency of bile salt, to initiate cholesterol crystal nucleation in the gallbladder with an impaired function. Those crystals grow to become macroscopic stones in the gallbladder mucin gel, accumulated under an arachidonate-prostanoid pathway induced-hypersecretion by the gallbladder wall. These events can be modified by bile salt supplementation, which provides a detergent action. Therefore, oral bile salt administration is a cost-effective, non-surgical therapy under certain circumstances. Understanding the pathogenesis of cholesterol gallstones attributes to the therapeutic guideline based upon scientific and clinical evidence.

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Carcinoembryonic antigen-related cell adhesion molecule 1 is the 85-kilodalton pronase-resistant biliary glycoprotein in the cholesterol crystallization promoting low density protein-lipid complex

Cited by 9 publications

References 34 publications

Cholesterol diet‐induced hyperlipidemia influences gene expression pattern of rat hearts: a DNA microarray study

Cholesterol diet‐induced hyperlipidemia influences gene expression pattern of rat hearts: a DNA microarray study

Human CEACAM1-LF regulates lipid storage in HepG2 cells via fatty acid transporter CD36

Recent understanding of cholesterol gallstone pathogenesis: implication to non-surgical therapeutic strategy

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