Effect of maternal cholestasis and treatment with ursodeoxycholic acid on the expression of genes involved in the secretion of biliary lipids by the neonatal rat liver

Macı́as, Rocı́o I.R.; Jiménez, Silvia; Serrano, Maria A.; Monte, María J.; Marin, José J.G.

doi:10.1016/j.lfs.2006.05.012

Cited by 11 publications

(17 citation statements)

References 25 publications

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“…Another possibility is that cholephilic compounds may exit the fetal liver via ATP-dependent pumps of the ABC family located in the basolateral plasma membrane. Supporting this concept is the higher expression of Mrp1 and Mrp3 in fetal than in maternal rat liver [38,42] .…”

Section: The Hepatobiliary Excretory Function During Intrauterine Lifementioning

confidence: 92%

“…The fact that the expression of export pumps, such as Mrp2 and Bsep, only appears in rat fetal liver in the last third of gestation [37,38] is probably the cause of the low efficiency of this route of excretion during pregnancy. As previously commented, the serum levels of bile acids and bile pigments are higher in the fetus than in the mother.…”

Section: The Hepatobiliary Excretory Function During Intrauterine Lifementioning

confidence: 99%

“…It is not known how cholephilic organic anions generated by the fetal liver reach the sinusoidal blood, but because some OATPs may act as bi-direction-al transporters [39][40][41] , they are good candidates for carrying out this function. Moreover, the expression of several OATP isoforms has been detected in rat fetal liver [38,42] . However, the abundance of these transporters in fetal liver is much lower than in adult liver, except for Oatp4a1 [43] and its human orthologue OATP4A1 [44] .…”

Section: The Hepatobiliary Excretory Function During Intrauterine Lifementioning

confidence: 99%

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Excretion of biliary compounds during intrauterine life

Macı́as¹,

Marin²,

Serrano³

2009

WJG

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In adults, the hepatobiliary system, together with the kidney, constitute the main routes for the elimination of several endogenous and xenobiotic compounds into bile and urine, respectively. However, during intrauterine life the biliary route of excretion for cholephilic compounds, such as bile acids and biliary pigments, is very poor. Although very early in pregnancy the fetal liver produces bile acids, bilirubin and biliverdin, these compounds cannot be efficiently eliminated by the fetal hepatobiliary system, owing to the immaturity of the excretory machinery in the fetal liver. Therefore, the potentially harmful accumulation of cholephilic compounds in the fetus is prevented by their elimination across the placenta. Owing to the presence of detoxifying enzymes and specific transport systems at different locations of the placental barrier, such as the endothelial cells of chorionic vessels and trophoblast cells, this organ plays an important role in the hepatobiliary-like function during intrauterine life. The relevance of this excretory function in normal fetal physiology is evident in situations where high concentrations of biliary compounds are accumulated in the mother. This may result in oxidative stress and apoptosis, mainly in the placenta and fetal liver, which might affect normal fetal development and challenge the fate of the pregnancy. The present article reviews current knowledge of the mechanisms underlying the hepatobiliary function of the fetal-placental unit and the repercussions of several pathological conditions on this tandem.

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Section: The Hepatobiliary Excretory Function During Intrauterine Lifementioning

confidence: 92%

Section: The Hepatobiliary Excretory Function During Intrauterine Lifementioning

confidence: 99%

Section: The Hepatobiliary Excretory Function During Intrauterine Lifementioning

confidence: 99%

See 1 more Smart Citation

Excretion of biliary compounds during intrauterine life

Macı́as¹,

Marin²,

Serrano³

2009

WJG

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“…Serrano et al used high doses of ursodeoxycholic acid to reduce clinical manifestations of ICP in the most severe cases without relevant side effects [78]. Papers dealing with the interaction between ursodeoxycholic acid and the pathogenetical background of ICP have proved that this drug can act preserving the trophoblast structure and the BA excretion pathways [79][80][81][82][83]. Ursodeoxycholic acid is the drug with the clearest evidence about usefulness and safety for ICP treatment also on the basis of a number of anecdotal series [84][85][86][87][88].…”

Section: Obstetric Management and Pharmacological Treatmentmentioning

confidence: 99%

Intrahepatic Cholestasis of Pregnancy and Bile Acids Induced Lung Injury in Newborn Infants

Zecca¹,

Luca²,

Marras³

et al. 2007

CPR

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Intrahepatic cholestasis of pregnancy (ICP) is a clinical syndrome of unknown pathophysiology, occurring during the second half of pregnancy and persisting until delivery. The incidence of ICP varies from 0.1% to 1.5% of pregnancies in Europe, North America and Australia and from 9.2% to 15.6% in South American countries such as Bolivia and Chile. This syndrome has been associated with increased foetal distress, intrauterine death, premature delivery, perinatal mortality and, more recently, with the occurrence of respiratory distress syndrome in the newborn infant. Bile acids (BA) are supposed to be the main mediators for these complications because ICP seriously impairs the placental clearance of foetal BA leading to a dangerous accumulation of these compounds within the foetus and the newborn. Cholestatic pregnancies have to be considered high risk ones, recent reports showing that BA can interfere with surfactant metabolism and are particularly harmful for the developing lung.This review summarizes existing literature data on this topic with particular emphasis on bile acids-induced lung injury. The authors discuss possible mechanisms of lung damage and highlight future research perspectives in this field.

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“…Liver Mrp1 mRNA expression in neonates is even higher when rats are treated with ursodeoxycholic acid during pregnancy (Macias et al, 2006). …”

Section: Regulation Of Hepatic Abcc1/mrp1 Transporter By Xenobiotics mentioning

confidence: 99%

Regulation of hepatic ABCC transporters by xenobiotics and in disease states

Manautou

2010

Drug Metabolism Reviews

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The subfamily of ABCC transporters consists of 13 members in mammals, including the multidrug resistance-associated proteins (MRPs), sulfonylurea receptors (SURs), and the cystic fibrosis transmembrane conductance regulator (CFTR). These proteins play roles in chemical detoxification, disposition, and normal cell physiology. ABCC transporters are expressed differentially in the liver and are regulated at the transcription and translation level. Their expression and function are also controlled by post-translational modification and membrane-trafficking events. These processes are tightly regulated. Information about alterations in the expression of hepatobiliary ABCC transporters could provide important insights into the pathogenesis of diseases and disposition of xenobiotics. In this review, we describe the regulation of hepatic ABCC transporters in humans and rodents by a variety of xenobiotics, under disease states and in genetically modified animal models deficient in transcription factors, transporters, and cell-signaling molecules.

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Effect of maternal cholestasis and treatment with ursodeoxycholic acid on the expression of genes involved in the secretion of biliary lipids by the neonatal rat liver

Cited by 11 publications

References 25 publications

Excretion of biliary compounds during intrauterine life

Excretion of biliary compounds during intrauterine life

Intrahepatic Cholestasis of Pregnancy and Bile Acids Induced Lung Injury in Newborn Infants

Regulation of hepatic ABCC transporters by xenobiotics and in disease states

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