Bibliographies thématiques / Biliary secretion

Littérature scientifique sur le sujet « Biliary secretion »

Auteur : Grafiati
Publié le 20 avril 2024

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Articles de revues sur le sujet "Biliary secretion"

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Blot-Chabaud, M., M. Dumont, M. Corbic et S. Erlinger. « Effect of acid-base balance on biliary bicarbonate secretion in the isolated perfused guinea pig liver ». American Journal of Physiology-Gastrointestinal and Liver Physiology 258, no 6 (1 juin 1990) : G863—G872. http://dx.doi.org/10.1152/ajpgi.1990.258.6.g863.

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Secretin-induced choleresis is of ductal origin and involves bicarbonate transport. Its mechanism is unknown. To determine the relative effects of systemic pH, PCO2, and bicarbonate concentration on secretin-stimulated bicarbonate transport, states of acute metabolic and respiratory acidosis or alkalosis were created in isolated perfused guinea pig livers with or without secretin infusion. During spontaneous secretion conditions, biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.62) or perfusate PCO2 (23.9-59.7) but was significantly correlated with perfusate bicarbonate concentration (17.5-37.9 mM). Under secretion infusion (25 mU/min), bile flow and biliary bicarbonate concentration increased significantly (109 and 51%, respectively). Biliary bicarbonate secretion was not correlated with perfusate pH (7.19-7.60) but was significantly correlated both with perfusate bicarbonate concentration (14.6-36.8 mM) and PCO2 (25.8-54.3 mmHg). Spontaneous and secretin-induced bile flow were correlated with biliary bicarbonate concentration. The correlation between biliary bicarbonate secretion and PCO2 during secretin-induced choleresis supports the hypothesis that secretin-induced biliary bicarbonate secretion could, at least in part, involve a transport of H+ (or OH-) rather than HCO3- itself and that intracellular pH could play a role in the regulation of this secretion. Amiloride (5 X 10(-4) M) did not influence secretin-induced biliary bicarbonate secretion. This result suggests that the Na(+)-H+ exchange is not involved in bicarbonate secretion by ductular cells.
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Uc, Aliye, Radhamma Giriyappa, David K. Meyerholz, Michelle Griffin, Lynda S. Ostedgaard, Xiao Xiao Tang, Marwa Abu-El-Haija et al. « Pancreatic and biliary secretion are both altered in cystic fibrosis pigs ». American Journal of Physiology-Gastrointestinal and Liver Physiology 303, no 8 (15 octobre 2012) : G961—G968. http://dx.doi.org/10.1152/ajpgi.00030.2012.

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The pancreas, liver, and gallbladder are commonly involved in cystic fibrosis (CF), and acidic, dehydrated, and protein-rich secretions are characteristic findings. Pancreatic function studies in humans have been done by sampling the jejunal fluid. However, it has been difficult to separately study the function of pancreatic and biliary systems in humans with CF, because jejunal fluid contains a mixture of bile and pancreatic fluids. In contrast, pancreatic and biliary ducts open separately into the porcine intestine; therefore, biliary and pancreatic fluid can be individually analyzed in CF pigs. We studied newborn wild-type (WT) and CF pigs and found that CFTR was localized to the pancreatic ducts. We collected bile and pancreatic fluid and analyzed pancreatic enzymes with activity assays and immunoblot. Pancreatic enzyme expression was significantly decreased in CF compared with WT pigs. The volume and pH of pancreatic fluid were significantly lower and protein concentration was >5-fold higher in CF pigs. Secretin stimulation increased pancreatic fluid volume and pH in WT, but not CF, pigs. Baseline bile volume did not differ between WT and CF pigs, but volume did not increase in response to secretin in CF pigs. Bile pH was lower and protein concentration was twofold higher in CF pigs. These results indicate that pancreatic and biliary secretions are altered in CF pigs. Abnormal pancreatic and biliary secretion in CF may have important implications in disease pathogenesis.
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Sætre, S. S., N. J. Andersen, T. Houe, P. Svendsen, J. F. Rehfeld, O. Olsen et O. B. Schaffalitzky de Muckadell. « Regulation of porcine biliary secretion by secretin ». Acta Physiologica Scandinavica 163, no 1 (mai 1998) : 113–19. http://dx.doi.org/10.1046/j.1365-201x.1998.00349.x.

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Alpini, G., R. Lenzi, W. R. Zhai, P. A. Slott, M. H. Liu, L. Sarkozi et N. Tavoloni. « Bile secretory function of intrahepatic biliary epithelium in the rat ». American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no 1 (1 juillet 1989) : G124—G133. http://dx.doi.org/10.1152/ajpgi.1989.257.1.g124.

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To shed light on ductular fluid secretion, hepatic histology and ultrastructure, cell proliferation and phenotypes, and several aspects of biliary physiology were studied in rats with ductular cell hyperplasia induced by either biliary obstruction (0-14 days) or 1-naphthylisothiocyanate (ANIT) feeding (0-28 days). In both groups of experimental animals, bile duct hyperplasia and spontaneous bile flow and secretin-induced choleresis increased with time of treatment in a linear fashion. Measurements of [14C]mannitol biliary entry and of biliary tree volume showed that the increase in both spontaneous and secretin-stimulated bile flow originated at the proliferated biliary structures. Ultrastructural examination, [3H]thymidine incorporation, and histochemical and immunohistochemical staining for various markers demonstrated that in both hyperplastic reactions the proliferated cells were the progeny of preexisting biliary epithelial cells and retained their characteristics. These results indicate that the increased bile secretory activity associated with either biliary obstruction or ANIT intoxication reflects a quantitative change due to the proliferation of biliary epithelial cells. Thus both models of bile ductular cell hyperplasia lend themselves to assessment of the transport function of intrahepatic biliary epithelium and its contribution to normal bile formation. In the present studies, we have estimated that net ductular secretion in the normal rat accounts for 10-13% of spontaneously secreted hepatic bile.
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Zeniya, M., et A. Reuben. « Triton WR-1339-induced changes in serum lipids and biliary lipid secretion ». American Journal of Physiology-Gastrointestinal and Liver Physiology 254, no 3 (1 mars 1988) : G346—G354. http://dx.doi.org/10.1152/ajpgi.1988.254.3.g346.

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Biliary lipid secretion rates were measured in fed rats after an intravenous injection of Triton WR-1339 (TWR, 60 mg/100 g body wt), an agent that inhibits lipoprotein removal from the circulation. Serum triglyceride, phospholipid (PL), and cholesterol (CH) concentrations rose within 3 h of TWR to 45, 6.6, and 10 times control values, respectively, at 24-36 h. Serum lipids fell rapidly at 48 h and were normal by 72-96 h after TWR. TWR did not alter bile flow, hepatic bile acid transport, or biliary bile acid output. Within 0.5 h of TWR, biliary PL and CH outputs fell greater than 70%, and taurocholate-stimulated biliary PL secretion was markedly reduced. Biliary PL and CH secretion rates were approximately 30 and approximately 40% suppressed, respectively, 24 h after TWR, 160 and 330% elevated, respectively, at 48 h, and normally by 72 h, despite normal taurocholate-stimulated biliary PL secretion. Biliary beta-glucuronidase secretion (a lysosomal enzyme) was unchanged for 3 h after TWR but was increased at 24, 48, and 72 h, independent of biliary lipid secretion. Thus TWR acutely dissociates bile acid from lipid secretion without impairing bile acid transport or biliary lysosomal discharge. Late changes in biliary lipid secretion relate closely to TWR-induced change in serum lipid metabolism but not to stimulation of biliary lysosomal discharge.
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Hofmann, Alan F. « Biliary Secretion : Future Perspectives ». Digestion 58, no 1 (1997) : 24–28. http://dx.doi.org/10.1159/000201519.

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Reuben, A., P. N. Maton, G. M. Murphy et R. H. Dowling. « Bile Lipid Secretion in Obese and Non-Obese Individuals with and without Gallstones ». Clinical Science 69, no 1 (1 juillet 1985) : 71–79. http://dx.doi.org/10.1042/cs0690071.

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1. Biliary lipid secretion rates were measured in non-obese and obese individuals with and without cholesterol gallstones, using a steady-state, amino acid duodenal perfusion method. In addition, biliary lipid secretion rates were measured in five obese gallstone patients receiving high-dose chenodeoxycholic acid therapy (16-22 mg day−1 kg−1). 2. Bile acid secretion rates in the non-obese patients with cholesterol gallstones (563+sem 70 μmol/h, n = 6) were significantly lower than in the non-obese controls (1078 + 210 μmol/h, n = 10, P < 0.05), whereas cholesterol secretion rates were similar in the non-obese individuals with and without gallstones (51+7 and 42+4 μmol/h respectively). 3. In the obese, both with and without gallstones, the major abnormality was hypersecretion of cholesterol (107+7 μmol/h, n = 7, and 81 + 15 μmol/h, n = 7, respectively). Both these values were significantly greater than those in the non-obese controls (P < 0.01-0.02). 4. Biliary cholesterol secretion rates correlated significantly with bile acid secretion rates but, for every mole of bile acid secreted, the obese secreted more cholesterol than the non-obese. 5. Chenodeoxycholic acid treatment lowered biliary cholesterol saturation in obese gallstone patients by reducing biliary cholesterol secretion. 6. These results suggest that there are two major types of defect in biliary lipid secretion in gallstone patients: reduced biliary bile acid secretion in non-obese gallstone patients and excessive biliary cholesterol secretion in the obese.
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Chanussot, F., H. Lafont, J. Hauton, B. Tuchweber et I. Yousef. « Studies on the origin of biliary phospholipid. Effect of dehydrocholic acid and cholic acid infusions on hepatic and biliary phospholipids ». Biochemical Journal 270, no 3 (15 septembre 1990) : 691–95. http://dx.doi.org/10.1042/bj2700691.

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The correlation between the secretion of biliary phospholipid (PL) and bile acid suggests a regulatory effect of bile acid on PL secretion. Bile acids may influence PL synthesis and/or the mobilization of a preformed PL pool. The objective of this study was to determine the contribution of these two sources to biliary PL, by using an experimental protocol in which dehydrocholic acid (DHCA) and cholic acid (CA) were infused to manipulate biliary PL secretion. In control rats, there was a steady state in bile flow. PL secretion and the biliary secretion of newly synthesized phosphatidylcholine (PC). The specific radioactivity of PC in bile was significantly higher than in plasma, microsomes and canalicular membranes. DHCA infusion decreased biliary PC secretion rate by 80%, and secretion returned to normal values at the transport maximum of CA. The specific radioactivity of biliary PC was decreased by 30% by DHCA infusion and reached normal values during CA infusion. There were no significant changes in the specific radioactivity of PC in plasma or cellular organelles during infusion of bile acids. These data indicate that: (1) newly synthesized PC contributes a small percentage to biliary PC; thus a preformed pool (microsomal and extrahepatic) is a major source of biliary PL; (2) the contribution of the extrahepatic pool to the biliary PL may be more important than the microsomal pool.
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Han, Yuyan, Paolo Onori, Fanyin Meng, Sharon DeMorrow, Julie Venter, Heather Francis, Antonio Franchitto et al. « Prolonged exposure of cholestatic rats to complete dark inhibits biliary hyperplasia and liver fibrosis ». American Journal of Physiology-Gastrointestinal and Liver Physiology 307, no 9 (1 novembre 2014) : G894—G904. http://dx.doi.org/10.1152/ajpgi.00288.2014.

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Biliary hyperplasia and liver fibrosis are common features in cholestatic liver disease. Melatonin is synthesized by the pineal gland as well as the liver. Melatonin inhibits biliary hyperplasia of bile duct-ligated (BDL) rats. Since melatonin synthesis (by the enzyme serotonin N-acetyltransferase, AANAT) from the pineal gland increases after dark exposure, we hypothesized that biliary hyperplasia and liver fibrosis are diminished by continuous darkness via increased melatonin synthesis from the pineal gland. Normal or BDL rats (immediately after surgery) were housed with light-dark cycles or complete dark for 1 wk before evaluation of 1) the expression of AANAT in the pineal gland and melatonin levels in pineal gland tissue supernatants and serum; 2) biliary proliferation and intrahepatic bile duct mass, liver histology, and serum chemistry; 3) secretin-stimulated ductal secretion (functional index of biliary growth); 4) collagen deposition, liver fibrosis markers in liver sections, total liver, and cholangiocytes; and 5) expression of clock genes in cholangiocytes. In BDL rats exposed to dark there was 1) enhanced AANAT expression/melatonin secretion in pineal gland and melatonin serum levels; 2) improved liver morphology, serum chemistry and decreased biliary proliferation and secretin-stimulated choleresis; and 4) decreased fibrosis and expression of fibrosis markers in liver sections, total liver and cholangiocytes and reduced biliary expression of the clock genes PER1, BMAL1, CLOCK, and Cry1. Thus prolonged dark exposure may be a beneficial noninvasive therapeutic approach for the management of biliary disorders.
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Verkade, H. J., R. Havinga, A. Gerding, R. J. Vonk et F. Kuipers. « Mechanism of bile acid-induced biliary lipid secretion in the rat : effect of conjugated bilirubin ». American Journal of Physiology-Gastrointestinal and Liver Physiology 264, no 3 (1 mars 1993) : G462—G469. http://dx.doi.org/10.1152/ajpgi.1993.264.3.g462.

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We have compared the effects of bilirubin and bilirubin ditaurate (BDT) on biliary phospholipid and cholesterol secretion in unanesthetized normal Wistar (NW) and Groningen Yellow (GY) Wistar rats under various experimental conditions. GY rats express a genetic defect in biliary secretion, but not in hepatic uptake, of various organic anions. Under physiological conditions, NW and GY rats showed similar biliary secretion rates of bile acids and of bilirubin, despite the fact that bilirubin concentrations in GY plasma were 25 times as high and in GY livers three times as high as in NW plasma and livers, respectively. Secretion of cholesterol and phospholipids was not impaired in GY rats under these conditions. Biliary secretion of intravenously injected BDT (3 mumol/100 g body wt) was delayed in eight-day bile-diverted GY rats and showed lower peak values when compared with NW rats. The inhibitory effects of BDT on phospholipid and cholesterol secretion paralleled these differences, being delayed and much less pronounced in GY rats. No overshoot in phospholipid or cholesterol secretion was observed when bilirubin output returned to preinjection values. Stimulation of [14C]choline-labeled phospholipid secretion after a bolus injection of taurochenodeoxycholic acid (1 mumol/100 g body wt) closely followed biliary bile acid concentration. Similarly, inhibition of labeled phospholipid secretion by BDT closely paralleled the biliary bilirubin concentration. Gel filtration studies (Sepharose 4B-CL) under micelle-preserving conditions demonstrated a specific interaction of BDT with biliary bile acids. The presented data indicate that conjugated bilirubin does not inhibit biliary lipid secretion via interaction with bile acids inside the hepatocyte.(ABSTRACT TRUNCATED AT 250 WORDS)
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Thèses sur le sujet "Biliary secretion"

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Baxter, Debbie Jane. « Molecular mechanisms of biliary lipid secretion ». Thesis, Liverpool John Moores University, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298908.

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Mareux, Elodie. « Pharmacothérapie ciblée des déficits en ABCB11 ». Electronic Thesis or Diss., université Paris-Saclay, 2021. http://www.theses.fr/2021UPASL083.

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ABCB11/BSEP (Bile Salt Export Pump) est exprimé à la membrane canaliculaire des hépatocytes. Sa fonction de transport d’acides biliaires dans la bile est essentielle à la sécrétion biliaire. Près de 400 variations du gène ABCB11 ont été identifiées et sont associées à des maladies hépatobiliaires rares, la plus sévère étant la cholestase intrahépatique progressive familiale de type 2 (PFIC2). L’efficacité des traitements médicaux est limitée. Par conséquent, une transplantation hépatique est indiquée avant l’âge adulte pour près de deux tiers des patients. Dans ce contexte, l’identification de thérapies alternatives est un enjeu capital.Cette thèse s’intéresse à la recherche de stratégies thérapeutiques personnalisées permettant de corriger les conséquences pathologiques de certaines variations d’ABCB11 identifiées chez des patients. Dans le cadre d’une stratégie de traitement par des molécules potentiatrices, nous avons étudié les variations A257V, G562D et T463I d’ABCB11 par modélisation moléculaire 3D. L’étude de l’expression et de la fonction de ces variants dans différents modèles cellulaires a confirmé que ces variations étaient responsables d’un défaut de fonction du transporteur Abcb11. L’ivacaftor (VX 770, Kalydeco®), approuvé cliniquement pour le traitement de la mucoviscidose, corrigeait le défaut d’activité de ces trois variants.Des effets similaires ont été observés avec les molécules GLPG1837, SBC040 et SBC219, connues comme potentiateurs de CFTR (Cystic Fibrosis Transmembrane conductance Regulator). Dans une optique de thérapie combinatoire, nous avons également mis en évidence la capacité de ces potentiateurs à corriger le défaut de fonction des variants R1090C et R1090W, produits potentiels de la translecture du variant non-sens R1090X. Nous avons également évalué les molécules correctrices elexacaftor (VX-445) et tezacaftor (VX-661). Ces correcteurs, en monothérapie ou en combinaison, permettaient de restaurer l’adressage du variant R1128C, s’accompagnant d’une augmentation significative du transport de taurocholate. De façon intéressante, l’addition de molécules potentiatrices réduisait ces effets.L’ensemble de ces travaux constitue une preuve de concept que les défauts de certains variants d’ABCB11 peuvent être corrigés par ces molécules potentiatrices à haut potentiel thérapeutique. Ce type de traitements pourrait être envisagé pour les patients atteints de déficit en ABCB11 et permettrait ainsi d’augmenter la pharmacopée disponible pour traiter ce genre de pathologies et ainsi repousser voir palier à la transplantation hépatique pour les cas les plus sévères
ABCB11/BSEP (Bile Salt Export Pump) is expressed at the canalicular membrane of hepatocytes. It ensures bile acids secretion into bile which is essential for biliary secretion. Nearly 400 variations of the ABCB11 gene have been identified and are associated with rare hepatobiliary diseases, the most severe being progressive familial intrahepatic cholestasis type 2 (PFIC2). The effectiveness of medical treatments is limited. Consequently, liver transplantation is required before adulthood for almost 2/3 of PFIC2 patients. In this context, the identification of alternative therapies is a major challenge.This thesis focuses on personalized therapeutic strategies to correct the pathological consequences of some ABCB11 variations identified in patients. The A257V, G562D and T463I variations of ABCB11 were studied by 3D molecular modelling. These variations were responsible for a defect in Abcb11 transport function. Ivacaftor (VX-770, Kalydeco®), a clinically approved cystic fibrosis treatment, corrects the activity defect of the three variants.Similar effects were observed with GLPG1837, SBC040 and SBC219, known as potentiators of CFTR (Cystic Fibrosis Transmembrane Conductance Regulator).From a combinatory therapy perspective, we also demonstrated the ability of these potentiators to correct the transport defect of the R1090C and R1090W variants, potential readthrough products of the R1090X nonsense variant. We also evaluated the ability of Elexacaftor (VX-445) and Tezacaftor (VX 661) correctors of CFTR. These correctors, alone or in combination, restored trafficking of the R1128C missense variant, leading to a significant increase in the transport function. Interestingly, the addition of potentiators abolishes this effect.Altogether, this thesis constitutes a proof of concept that molecules with high therapeutic potential can correct the molecular defects of ABCB11 variants. These treatments could increase the pharmacopoeia available for patients with ABCB11 deficiency and thus delay or even suppress the need for liver transplantation
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LANGLOIS, ANNIK. « Contribution a l'etude de la regulation hormonale des secretions digestives chez le porc : effets du polypeptide pancreatique sur la secretion pancreatique exocrine et la secretion biliaire chez l'animal conscient ». Paris 7, 1989. http://www.theses.fr/1989PA077080.

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Lam, Pak-yan Ian, et 林柏炘. « Secretin in biliary physiology : autocrine regulation on cholangiocyte proliferation and negative feedbackregulation on duodenal secretin expression via bile acids ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hub.hku.hk/bib/B43572327.

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Lam, Pak-yan Ian. « Secretin in biliary physiology autocrine regulation on cholangiocyte proliferation and negative feedback regulation on duodenal secretin expression via bile acids / ». Click to view the E-thesis via HKUTO, 2009. http://sunzi.lib.hku.hk/hkuto/record/B43572327.

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Zanninelli, Giuliana. « Effets de chelateurs sur le routage cellulaire du fer non lie a la transferrine (doctorat : biologie et sciences de la sante) ». Rennes 1, 2000. http://www.theses.fr/2000REN1B044.

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Dupuy-Esnault, Christine. « Relation entre le cholestérol libre des HDL et des LDL et la secretion biliaire du cholestérol et des sels biliaires : influence de divers régimes hyperlipidiques ». Aix-Marseille 2, 1986. http://www.theses.fr/1986AIX22066.

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Bruneau, Alix. « Régulation de l'expression membranaire du transporteur de phospholipides biliaires ABCB4 : effet de mutations Functional Defect of Variants in the Adenosine Triphosphate–Binding Sites of ABCB4 and Their Rescue by the Cystic Fibrosis Transmembrane Conductance Regulator Potentiator, Ivacaftor (VX-770) Structural analogues of roscovitine rescue the intracellular traffic and the function of ER-retained ABCB4 variants in cell models ». Thesis, Sorbonne université, 2019. http://www.theses.fr/2019SORUS048.

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ABCB4 est exprimé à la membrane canaliculaire des hépatocytes où il sécrète un composant majeur de la bile : la phosphatidylcholine. Plus de 500 mutations d’ABCB4 sont associées à des maladies biliaires. La pathologie la plus sévère est la PFIC3, qui se développe tôt dans l’enfance et progresse rapidement vers l’insuffisance hépatique. La transplantation hépatique reste la seule thérapie efficace. Le développement d’alternatives représente donc un enjeu majeur. Cette thèse s’intéresse à l’effet de cinq mutations décrites chez des patients et situées dans les sites de liaison à l’ATP d’ABCB4. En combinant la modélisation 3D avec des études in vitro, nous avons montré que ces mutations sont responsables d’un défaut d’activité d’ABCB4. Nous avons mis en évidence que le VX-770, un médicament approuvé en clinique pour traiter les patients atteints de mucoviscidose, restaure l’activité des cinq mutants. Ces travaux ouvrent des perspectives de repositionnement du VX-770 pour le traitement ciblé de patients atteints de pathologies biliaires liées à ABCB4. La seconde partie de cette thèse consiste à étudier le rôle de l’interaction du domaine N-terminal d’ABCB4 avec la kinase MRCKalpha. L’inhibition ou l’extinction de cette kinase montrent que MRCKalpha joue un rôle dans la régulation de l’expression membranaire d’ABCB4 en contrôlant son internalisation depuis la membrane plasmique. En inhibant la protéine MLC2, effecteur de MRCKa, nous avons ensuite montré que l’effet de MRCKalpha sur l’expression d’ABCB4 passe par MLC2, qui est un partenaire du domaine linker d’ABCB4. Notre travail montre un rôle commun de ces deux partenaires dans la régulation de l’internalisation d’ABCB4
ABCB4 is exclusively expressed at the canalicular membrane of hepatocytes where its function is to translocate phosphatidylcholine (PC) into bile. Variations in ABCB4 gene sequence are associated with several chronic and progressive liver diseases. The most severe is PFIC3 which develops early in childhood and most often requires liver transplantation. Less severe diseases are the intrahepatic cholestasis of pregnancy and the low phospholipid- associated cholelithiasis syndrome which occur in young adults. Up to now, about 500 disease-causing ABCB4 variants have been reported. A challenge is to find pharmacological treatments for the severe forms of the diseases. We have studied the effect of five disease-causing variations that reside in the highly conserved motifs of ABC transporters, involved in ATP binding. Using three-dimension structural modeling and in vitro studies, we showed that the five mutants were normally processed and targeted to the plasma membrane, whereas their PC secretion activity was dramatically decreased. PC secretion activity of the mutants was rescued by the clinically approved CFTR potentiator ivacaftor (VX-770). These results pave the way for personalized therapy in ABCB4-related diseases.The second part of my project was aimed at investigating the potential role of two ABCB4 partners, the kinase MRCKalpha and its effector the myosin light chain II (MLCII) in the expression and function of ABCB4. We found that downregulation of both partners didn’t affect the canalicular localization of ABCB4 but led to a reduction of its endocytosis. Our results open new insights into the mechanisms underlying the regulation of ABCB4 expression and function
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Sutherland, Jessica Elin. « The kinetics of absorption, tissue distribution, biliary secretion, and urinary excretion of ingested aluminum ». 1997. http://catalog.hathitrust.org/api/volumes/oclc/40160453.html.

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Mustacich, Debbie J. « The microtubule system and the canalicular mdr2 P-glycoprotein play a role in the intracellular transport and biliary secretion of ��-Tocopherol and phosphatidylcholine in rats and mice ». Thesis, 1998. http://hdl.handle.net/1957/34062.

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Livres sur le sujet "Biliary secretion"

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Hamlin, Sandra Mary. Modulation of biliary lipid secretion. Birmingham : University of Birmingham, 1990.

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Mustacich, Debbie J. The microtubule system and the canalicular mdr2 P-glycoprotein play a role in the intracellular transport and biliary secretion of Ü-Tocopherol and phosphatidylcholine in rats and mice. 1998.

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Chapitres de livres sur le sujet "Biliary secretion"

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Zimniak, Piotr, et Roger Lester. « Disorders of Biliary Secretion ». Dans Molecular Biology of Membrane Transport Disorders, 519–39. Boston, MA : Springer US, 1996. http://dx.doi.org/10.1007/978-1-4613-1143-0_26.

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Carulli, Nicola, Paola Loria, Marco Bertolotti et Alberto Tripodi. « Determinants of Biliary Cholesterol Secretion ». Dans Assessment and Management of Hepatobiliary Disease, 49–58. Berlin, Heidelberg : Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-72631-6_7.

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Coleman, R., K. L. Rahman, M. E. Bellringer et M. Carrella. « Biliary Lipid Secretion and its Control ». Dans Bile Acids in Health and Disease, 43–60. Dordrecht : Springer Netherlands, 1988. http://dx.doi.org/10.1007/978-94-009-1249-6_4.

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Kuipers, Folkert, Ronald P. J. Oude Elferink, Henkjan J. Verkade et Albert K. Groen. « Mechanisms and (Patho)Physiological Significance of Biliary Cholesterol Secretion ». Dans Subcellular Biochemistry, 295–318. Boston, MA : Springer US, 1997. http://dx.doi.org/10.1007/978-1-4615-5901-6_11.

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Lirussi, F., et L. Okolicsanyi. « The Effect of Drugs on Liver Function and Biliary Secretion ». Dans Biochemical Pharmacology as an Approach to Gastrointestinal Disorders, 239–47. Dordrecht : Springer Netherlands, 1997. http://dx.doi.org/10.1007/978-94-011-5390-4_19.

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Barbara, L., G. Mazzella, N. Villanova, P. Simoni, M. Ronchi, A. Roda, E. Roda et F. Bazzoli. « Effect of Gemfibrozil Administration on Biliary Lipid Secretion : A Crossover Study with Clofibrate ». Dans Drugs Affecting Lipid Metabolism, 350–54. Berlin, Heidelberg : Springer Berlin Heidelberg, 1987. http://dx.doi.org/10.1007/978-3-642-71702-4_65.

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Bentham Science Publisher, Bentham Science Publisher. « Biliary Secretion ». Dans FFunctional Molecular Imaging In Hepatology (Open Access), 49–75. BENTHAM SCIENCE PUBLISHERS, 2012. http://dx.doi.org/10.2174/978160805290511201010049.

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Pal, Gopal, Pravati Pal et Nivedita Nanda. « Biliary Secretion ». Dans Comprehensive Textbook of Medical Physiology (Volume 1), 378. Jaypee Brothers Medical Publishers (P) Ltd., 2017. http://dx.doi.org/10.5005/jp/books/12960_43.

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Feher, Joseph. « Pancreatic and Biliary Secretion ». Dans Quantitative Human Physiology, 810–20. Elsevier, 2017. http://dx.doi.org/10.1016/b978-0-12-800883-6.00080-x.

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Miller, Laurence J. « Gallbladder and Biliary Secretion ». Dans Encyclopedia of Endocrine Diseases, 94–96. Elsevier, 2004. http://dx.doi.org/10.1016/b0-12-475570-4/00497-2.

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