Relevant bibliographies by topics / Biliary epithelium

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Biliary epithelium'

Author: Grafiati
Published: 9 March 2023
Last updated: 10 March 2023

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Journal articles on the topic "Biliary epithelium"

1

Alpini, G., R. Lenzi, W. R. Zhai, P. A. Slott, M. H. Liu, L. Sarkozi, and N. Tavoloni. "Bile secretory function of intrahepatic biliary epithelium in the rat." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 1 (July 1, 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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Katabi, Nora. "Neoplasia of Gallbladder and Biliary Epithelium." Archives of Pathology & Laboratory Medicine 134, no. 11 (November 1, 2010): 1621–27. http://dx.doi.org/10.5858/2009-0580-rar.1.

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Abstract Context.—Diagnosis of biliary neoplasia can be challenging but is essential for the appropriate clinical management of patients. Therefore, it is important to recognize the morphologic features of the biliary neoplasms to report a correct diagnosis. Objectives.—(1) To discuss the differential diagnosis of dysplasia in the gallbladder and differentiate dysplasia from reactive atypia and invasive carcinoma, (2) review the histologic features of adenoma and polypoid biliary lesions, (3) highlight the differential diagnosis of adenocarcinoma in liver biopsy, and (4) discuss the differential diagnosis of atypical biliary glandular lesions. Data Sources.—Current English literature related to gallbladder and biliary neoplasia. Conclusions.—Biliary glandular neoplasms show a wide spectrum of morphology and have many mimics. Careful examination of the histologic features of these lesions and familiarity with their morphology can help to achieve the correct diagnosis.
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3

Fava, Giammarco, Shannon Glaser, Heather Francis, and Gianfranco Alpini. "The Immunophysiology of Biliary Epithelium." Seminars in Liver Disease 25, no. 03 (August 2005): 251–64. http://dx.doi.org/10.1055/s-2005-916318.

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4

Nguyen, N. Thao T., Theresa R. Harring, Laurie Holley, John A. Goss, and Christine A. O’Mahony. "Biliary Adenofibroma with Carcinoma In Situ: A Rare Case Report." Case Reports in Hepatology 2012 (2012): 1–3. http://dx.doi.org/10.1155/2012/793963.

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This case report exhibits a rare biliary tumor within the liver of a 53-year-old Caucasian woman. This exophytic, multicystic, 6.5×5.0 cm mass was composed of complex tubulocystic structures lined by nonmucin-secreting, biliary epithelium embedded in fibrous stroma, consistent with biliary adenofibroma. This is the seventh case described in the literature. Multiple foci of high-grade dysplasia/carcinoma in situ were found with a microscopic focus of invasive carcinoma in review of the pathology, making this only the second case reporting malignant transformation. It is presented to illustrate the premalignant potential in a biliary epithelial tumor currently categorized as benign.
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Li, Daneng, Ya-Han Zhang, Christiana J. Crook, and Renuka V. Iyer. "Updates in Biliary Tract Cancers." Cancers 14, no. 11 (June 1, 2022): 2746. http://dx.doi.org/10.3390/cancers14112746.

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Park, Ji-Won, Jung-Hee Kim, Sung-Eun Kim, Jang Han Jung, Myoung-Kuk Jang, Sang-Hoon Park, Myung-Seok Lee, Hyoung-Su Kim, Ki Tae Suk, and Dong Joon Kim. "Primary Biliary Cholangitis and Primary Sclerosing Cholangitis: Current Knowledge of Pathogenesis and Therapeutics." Biomedicines 10, no. 6 (May 31, 2022): 1288. http://dx.doi.org/10.3390/biomedicines10061288.

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Cholangiopathies encompass various biliary diseases affecting the biliary epithelium, resulting in cholestasis, inflammation, fibrosis, and ultimately liver cirrhosis. Primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC) are the most important progressive cholangiopathies in adults. Much research has broadened the scope of disease biology to genetic risk, epigenetic changes, dysregulated mucosal immunity, altered biliary epithelial cell function, and dysbiosis, all of which interact and arise in the context of ill-defined environmental triggers. An in-depth understanding of the molecular pathogenesis of these cholestatic diseases will help clinicians better prevent and treat diseases. In this review, we focus on the main underlying mechanisms of disease initiation and progression, and novel targeted therapeutics beyond currently approved treatments.
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Glaser, Shannon. "Heterogeneity of the intrahepatic biliary epithelium." World Journal of Gastroenterology 12, no. 22 (2006): 3523. http://dx.doi.org/10.3748/wjg.v12.i22.3523.

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Strazzabosco, Mario, Carlo Spirlì, and Lajos Okolicsanyi. "Pathophysiology of the intrahepatic biliary epithelium." Journal of Gastroenterology and Hepatology 15, no. 3 (March 10, 2000): 244–53. http://dx.doi.org/10.1046/j.1440-1746.2000.02091.x.

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9

Morell, Carola M., Luca Fabris, and Mario Strazzabosco. "Vascular biology of the biliary epithelium." Journal of Gastroenterology and Hepatology 28 (July 15, 2013): 26–32. http://dx.doi.org/10.1111/jgh.12022.

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10

Allen, Steven R., Mubeen Jafri, Bryan Donnelly, Monica McNeal, David Witte, Jorge Bezerra, Richard Ward, and Gregory M. Tiao. "Effect of Rotavirus Strain on the Murine Model of Biliary Atresia." Journal of Virology 81, no. 4 (November 22, 2006): 1671–79. http://dx.doi.org/10.1128/jvi.02094-06.

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ABSTRACT Biliary atresia is a devastating disorder of the newborn in which afflicted infants develop inflammation and fibrosis of the extrahepatic biliary tract, resulting in cirrhosis and end-stage liver disease. Infection with a virus is thought to be a contributing factor in the etiology of biliary atresia. In the murine model of biliary atresia, perinatal exposure to rhesus rotavirus (RRV) results in biliary epithelial cell infection causing bile duct obstruction. The purpose of this study was to determine if tropism for the biliary epithelial cell was unique to RRV. Newborn mice underwent intraperitoneal injection with five strains of rotavirus: RRV (simian), SA11-FM (simian/bovine), SA11-SM (simian), EDIM (murine), and Wa (human). RRV and SA11-FM caused clinical manifestations of bile duct obstruction and high mortality. SA11-SM caused clinical signs of hepatobiliary injury but the mortality was markedly reduced. EDIM and Wa caused no sign of hepatobiliary disease. The systemic and temporal distribution of viral protein and live virus varied according to the injected strain. Immunohistochemistry revealed that RRV and SA11-FM targeted the biliary epithelial cells. In contrast, SA11-SM was found in the liver but in not in the biliary epithelium. These results indicate that strain-specific characteristics dictate tropism for cells of hepatobiliary origin which in turn impact the ability to induce the murine model of biliary atresia.
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Dissertations / Theses on the topic "Biliary epithelium"

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Raven, Alexander Philip. "Impairing hepatocyte regeneration to determine the regenerative capacity of the biliary epithelium." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31177.

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Liver injury stimulates hepatocyte proliferation, regenerating the liver through self-replication. In cases where there is severe, repetitive, parenchymal damage, as seen in human chronic liver disease, hepatocyte mediated regeneration becomes impaired. In this setting it is currently unclear whether endogenous biliary epithelial cells can repopulate the hepatocyte compartment. This thesis therefore aimed to address this point by lineage tracing the main two liver epithelia populations on a background of impaired hepatocyte regeneration. To impair regeneration, an Itgb1 transgene was specifically deleted, conditionally, from the hepatocyte epithelium. Long-term loss of β1-Integrin alone or with additional injury caused an epithelial ductular reaction of biliary origin. Alongside β1-Integrin ablation, the hepatocyte epithelium was also labelled with a heritable ROSA26LSLtdTomato reporter. Impaired hepatocyte regeneration mediated by β1- integrin ablation resulted in 25% of hepatocytes becoming tdTomato negative (non-hepatocyte derived). To verify that the non-hepatocyte mediated regeneration was originating from the biliary epithelium, anti-Itgb1 RNAi was administrated to K19CreERT LSLtdTomato mice. Resulting in tdTomato positive hepatocytes that had differentiated from the labelled tdTomato positive biliary epithelial cells. In summary, this thesis demonstrates that hepatocyte β1-Integrin ablation combined with toxic damage causes marked ductular reactions and results in a substantial regeneration of functional hepatocytes from the biliary epithelium.
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SCIRPO, ROBERTO. "Activation of PPAR-gamma signaling as a novel target to limit nfkb-dependet in flammation in cystic fibrosis biliar epithelium." Doctoral thesis, Università degli Studi di Milano-Bicocca, 2014. http://hdl.handle.net/10281/50586.

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Cystic fibrosis-associated liver disease (CFLD) is a chronic cholangiopathy that negatively impacts the quality of life and survival of patients with Cystic Fibrosis (CF). CF is a disease of secretory epithelia caused by genetically-determined defective function of CFTR (cystic fibrosis conductance regulator), a cAMP-activated Cl- channel that, in the liver, is uniquely expressed in the biliary epithelium. The pathogenesis of CFLD is thought to be related to the ductal cholestasis caused by the defective channel function of CFTR. However, a number of evidence indicate that, in association with the genetic defect, other pathogenetic factors concur to determine the liver phenotype. During the first year of my doctorate we have demonstrated that in CFTR-defective biliary epithelium, exposed to bacterial-derived endotoxins, TLR4/NF-kB-dependent innate immune responses are increased, indicating a loss of “endotoxin tolerance”. The current standard of care for CFLD is limited to the administration of choleretic agents. Based on our novel interpretation of the pathogenesis of CFLD, a rational therapeutic approach to the management of CFLD should be to target the exaggerated inflammatory response of the biliary epithelium. Nuclear receptors (NRs), ligand-activated transcription factors that regulate several intracellular metabolic functions by controlling the expression of specific target genes, are now emerging as important regulators of inflammation in several conditions. In this work we sought to investigate the ability of NRs to modulate the TLR4/NF-kB-dependent innate immune responses in CF biliary epithelia. Our data indicate that cholangiocytes express several subtypes of NRs, including Peroxisome Proliferator Activated Receptor (PPAR) subgroup α, γ and β/δ, Liver X Receptors (LXR) subgroup β, Farnesoid X Receptor (FXR) and Vitamin D Receptor (VDR). Among these NRs, PPAR-γ was barely expressed in wild type (WT) cholangiocytes , but its expression, both at the gene and protein levels, was strongly and significantly more expressed in CF cells. In spite of its increased expression in the nucleus, PPAR-γ was not transcriptionally active in CF cholangiocytes; in fact the basal level of expression of PPAR-γ target genes (Acaa1b, Angptl4 and Hmgcs2) was similar to WT cholangiocytes. On the other hand, treatment of CF cholangiocytes with the PPAR-γ agonist pioglitazone significantly increased the expression of its target genes, indicating that the transcriptional activity of nuclear PPAR-γ could be readily activated in the presence of proper agonists. Consistent with the higher expression level of the receptor, the increase in PPAR-γ target genes stimulated by pioglitazone was higher in CF than in WT cholangiocytes. The observation that PPAR-γ, while inactive at baseline levels, was able to respond to exogenous stimulation, indicates that a defect in the availability of endogenous PPAR-γ activators might impair PPAR-γ function in CF and increase the receptor expression as counter-regulatory mechanism. Thus, to study the availability of endogenous PPAR-γ activators in CF, we performed lipidomic analysis of extracts from cultured cholangiocytes, and quantified the major ω-3 and ω-6 polyunsaturated fatty acids (PUFAs), i.e. the precursors of the active form of PPAR-γ ligands. We detected an increased ratio between arachidonic acid and docosahexaenoic acid (AA/DHA) and between arachidonic acid and linoleic acid (AA/LA) in CF cells compared to their controls. LA, the precursor of AA, is the main source of pro-inflammatory mediators, while DHA is an important precursor of anti-inflammatory eicosanoids that are able to activate PPAR-γ. This finding might explain, at least in part, the increased receptor expression in CF biliary cells. Having shown that CF cells express higher amounts of PPAR-γ, that can be activated by exogenous ligands, but it is not transcriptionally active because of the lack of endogenous ligands, we next tested if exogenous activation of PPAR-γ by synthetic ligands, might decrease the TLR4/NF-kB-driven inflammation in CFTR-defective biliary epithelium. We found that in Cftr-KO cells, in the presence of pioglitazone, nuclear translocation of p65/NF-kB, as well as its transcriptional activity, were significantly inhibited, both before and after stimulation with bacterial LPS. Moreover, the gene expression and protein secretion of several NF-kB-dependent pro-inflammatory cytokines, such as LIX (LPS-induced CXC chemokine), MCP-1 (monocyte chemotactic protein-1), MIP-2 (macrophage inflammatory protein 2), G-CSF (granulocyte colony-stimulating factor) and KC (keratinocyte chemo-attractant) were significantly inhibited both at baseline and after LPS stimulation. The anti-inflammatory effect of pioglitazone was the result of a direct activation of PPAR-γ receptor, as shown by reversal of pioglitazone-induced protection in the presence of the PPAR-γ antagonist GW9662. Finally, to understand the mechanism by which ligand-activated PPAR-γ blocks inflammation in CF cholangiocytes we analyzed the effect of pioglitazone on NF-kB activation pathway steps, and found that pioglitazone up-regulated IkB-α, a negative regulator of NF-kB. In conclusion, our results indicate that a decreased PPAR-γ function caused by a decreased availability of PPAR-γ endogenous agonists might be responsible for the chronic inflammatory state of CFTR-defective cholangiocytes. Stimulation of PPAR-γ signaling by the agonist pioglitazone is able to decrease NF-kB-dependent inflammatory responses by increasing IkB-α, thus may represent a novel strategy to limit inflammation in CFLD. Studies in mice models of liver damage in CFLD have been planned and may represent a proof of concept for anti-inflammatory treatment in CF.
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Maxwell, John Perry. "Carcinoembryonic antigen (CEA) in the extrahepatic biliary tract : investigation of its function and localisation in benign and malignant epithelium." Thesis, Queen's University Belfast, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388237.

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4

Godoy, Torres Valeria. "Implicaciones del Purinoma en la Biología y Patología del Epitelio Biliar." Doctoral thesis, Universitat de Barcelona, 2013. http://hdl.handle.net/10803/133312.

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El purinoma está formado por la red de proteínas de membrana que median el efecto biológico final de la adenosina (Ado) extracelular y sus metabolitos (ATP, ADP y AMP). Sus componentes actúan de forma sinérgica y concertada para iniciar, mantener y terminar la señal purinérgica. Los elementos que conforman esta red son: los receptores purinérgicos P1 de adenosina, los receptores purinérgicos P2 para ATP y ADP, las ATP/ADPasas (nucleotidasas) responsables de la degradación extracelular del ATP y ADP, y los transportadores de nucleósidos equilibrativos (ENTs) y concentrativos (CNTs) encargados del reciclaje de la adenosina. Los colangiocitos son células epiteliales que conforman el tracto biliar intra y extrahepático y se distribuyen en una red tridimensional de ductos interconectados. Su principal función es la de sensar y modificar la composición de la bilis proveniente de los cálculos biliares. Pero también participan junto a los hepatocitos en la detoxificación de xenobióticos. A un cuando los principales mecanismos efectores de estas funciones están directamente relacionados con el ATP extracelular y activación de los receptores P2, nada ha sido descrito para el resto de los componentes del purinoma. En los últimos años, el interés en el estudio de la fisiología de los colangiocitos ha aumentado significativamente debido al incremento progresivo en la incidencia de las enfermedades hepáticas colestásicas y del cáncer de tracto biliar a nivel mundial. El colangiocarcinoma (CC) proveniente de la transformación neoplásica de los colangiocitos, es el principal cáncer de conducto biliar. Debido a que es un cáncer de detección tardía, la principal opción para el tratamiento es la quimioterapia. Entre los agentes quimioterapéuticos más estudiados para su uso en monoterapia se encuentran derivados de uracilo como el 5‐Fluoruracilo (5‐FU), o derivados de nucleósidos como la citidina (gemcitabina), o de la uridina (capecitabina); también se utilizan agentes como el Cisplatino. Estos fármacos se utilizan también en combinaciones para aumentar la efectividad de la terapia. A pesar de que en otros modelos epiteliales humanos se ha demostrado que el transporte de los quimioterápicos, análogos de nucleósidos, al interior celular se hace por medio de NT, en la actualidad no existe ninguna evidencia ni de los mecanismos de entrada, ni de las entidades que median estos procesos en CC o en modelos no tumorales de colangiocitos. Los resultados principales de esta tesis muestran la presencia funcional de nuevos elementos del purinoma tanto en colangiocitos de rata, como en líneas celulares humanas de CC. En el modelo fisiológico de colangiocitos, describimos un crosstalk específico entre los transportadores de adenosina (CNT3 y CNT2), el receptor de alta afinidad para adenosina (A2A) y el receptor de ATP (P2Y2). Estos resultados indican que los receptores A2A y P2Y2, a través de un mecanismo dependiente de la vía intracelular dependiente de cAMP/PKA/ERK/CREB, están controlando la actividad de CNT3 y CNT2 y por lo tanto la recaptación de adenosina. Adicionalmente, confirmamos por primera vez que la entrada de la adenosina es diferencialmente modulada por los principales estímulos secretores del colangiocito (secretina y ATP). En el segundo capítulo, describimos los resultados del estudio extensivo de la expresión y actividad de los transportadores de nucleósidos en 8 biopsias humanas con diagnóstico confirmado de CC y en 8 líneas celulares humanas de CC, para la evaluación de cambios en la expresión luego de la exposición a diferentes régimenes de tratamientos con fármacos utilizados en la terapia del CC. Para complementar estos resultados también analizamos la expresión basal de 40 genes involucrados en la captación, metabolización y salida de estos fármacos. Los principales resultados revelaron que la expresión de MRP3 y OATP3 podrían correlacionar con la respuesta a la quimioterapia del CC.
The purinoma is the molecular network that mediates the final effects of the extracellular adenosine and its metabolites. The components of this network are: P1 receptors for adenosine, P2 receptors for ATP/ADP, the ATP/ADPasas responsible for extracellular degradation of ATP, and the equilibrative (ENTs) and concentrative (CNTs) nucleoside tranporters responsible for the recycling of adenosine. Cholangiocytes are epithelial cells that form the intra and extrahepatic biliary tract. In recent years, interest in the study of the physiology of cholangiocytes has increased signicantly due to the progressive increment in the incidence of cholestatic liver diseases and cholangiocarcinoma (CC) worldwide. The nucleoside‐derivatives drugs; 5‐Fluorouracil and gemcitabine, are the principal therapy indicated for the treatment of CC. Although in other human epithelial models have been shown that transport of nucleosideanalogues drugs into the cell is done by means of the nucleoside transporters, at the moment there is no evidence of the uptake mechanisms, nor the proteins that mediate these processes in CC or in non‐tumor models of the biliary epithelia. The principal results in this thesis showed the presence of new elements of the purinome in both rat cholangiocytes and in human CC cell lines. In the physiologic model of cholangiocytes we found a specific crosstalk between the adenosine transporters (CNT3 and CNT2), the adenosine A2A receptor and the P2Y2 receptor. Our key findings indicated that A2A and P2Y2 receptors, which trough a mechanism dependent of the cAMP/PKA/ERK/CREB axis, are controlling the activity of CNT3 and CNT2 and thus the cellular uptake of adenosine. Additionally, for the first time we confirmed that adenosine transport is differentially modulated by the main secretory stimuli described in cholangiocytes (secretin and ATP). We also performed an extensive study of the expression and activity of the nucleoside transporters in 8 cell lines and in 8 human biopsies of CC, evaluating changes after the exposure to different cancer drugs. We also analyzed the basal expression of 40 genes involved in the uptake, metabolism and extrusion of these drugs. The principal results of this approach revealed that the expression of MRP3 and OATP3 would possibly correlate with the response to the chemotherapy in CC.
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Flynn, Diana Mary. "Isolation and characterisation of biliary epithelial cells in extrahepatic biliary atresia." Thesis, University of Birmingham, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.433626.

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Chignard, Nicolas. "Bile Salts and Nuclear Receptors in Biliary Epithelial Cell Pathophysiology." Habilitation à diriger des recherches, Université Pierre et Marie Curie - Paris VI, 2012. http://tel.archives-ouvertes.fr/tel-00726374.

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The biliary epithelium is organized as a single layer of biliary epithelial cells (BECs) lining the biliary tree. BECs have three major biological functions: protection, secretion and proliferation. These functions may all be controlled by bile salts, the main constituents of bile. We therefore determined if human gallbladder-derived BECs exhibited bile salt transport activities that affect their secretory functions. We could show that the apical bile acid sodium- dependent transporter (ASBT) is expressed and functional in primary cultures of human BECs. Once transported inside BECs, bile salts stimulate chloride and mucin secretion through intracellular pathways linked to calcium. In BECs, the secretion process is however mainly elicited by membrane receptors that signal through the intracellular second messenger cAMP. We could show in a subsequent study that bile salts potentiate cAMP-regulated secretion in BECs by stimulating adenylyl cyclase activity through PKC α and δ. One of the most potent bile secretagogues is the vasoactive intestinal peptide, which exerts its effects through the vasoactive intestinal peptide receptor-1 (VPAC1). We have shown that VPAC1 is expressed in all major cell types participating in bile formation in humans (i.e. hepatocytes, intrahepatic and gallbladder biliary epithelial cells). Moreover, VPAC1 displays a gradient of expression along the human biliary tree, the gallbladder showing the highest level of expression. Interestingly, we could show that bile salts regulate VPAC1 expression in BECs through the farnesoid X receptor (FXR), indicating that bile salts may also regulate BECs secretion through transcriptional control. The secretory activities of BECs may be seen as a protective mechanism avoiding excessive exposure to toxics, such as endotoxins. We have shown that bile salts may also exert protection by controlling the expression of the antimicrobial peptide cathelicidin. Bile salts induced cathelicidin expression through two distinct nuclear receptors, FXR and the vitamin D nuclear receptor (VDR). Taken together, our results indicate that bile salts control BECs biological functions through post-traductional and transcriptional control. The involvement of VDR in the control of BECs biology may be of particular interest because VDR hepatic expression is restricted to non-parenchymal liver cells, such as BECs or resident hepatic macrophages (i.e. Kupffer cells).
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Parola, Maurizio. "Biochemical studies on biliary epithelial cells isolated from rat liver." Thesis, Brunel University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484102.

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Bratti, Maria Paz Leon. "Investigation of the immunogenicity of human intrahepatic biliary epithelial cells." Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.319181.

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Ayres, Reuben Christopher Simon. "In vitro investigation into the role of human intrahepatic biliary epithelial cells as targets in primary biliary cirrhosis." Thesis, University of Southampton, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296245.

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Brain, John George. "Investigation of injury and pharmacological modulation of biliary epithelial cells in ductopenic disease." Thesis, University of Newcastle upon Tyne, 2014. http://hdl.handle.net/10443/2437.

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Senescence and its associated secretory phenotype have been investigated in several vanishing bile duct syndromes. The current study evaluated the presence of senescent biliary epithelial cells (BEC) in acute cellular rejection of human liver allografts to ascertain whether senescent cells contribute to human disease progression in liver transplantation. There was a significant correlation between senescent BEC and grade of rejection. Furthermore there was a significant correlation between grade of rejection and BEC undergoing epithelial to mesenchymal transition (EMT). There was never any overlap between senescence and EMT markers in BEC. Further investigation of the association between senescence and EMT in vitro using both primary and immortalised human BEC exposed to oxidative stress showed, for the first time, that TGF-­b2 is part of the Senescence Associated Secretory Phenotype (SASP) in liver disease. Blockade of TGF-­b signalling by inhibition of the TGFbR, prevented any of the oxidative stress-­induced changes in BEC. Blockade of integrin aVb6 integrin also showed a variable ability to prevent TGF-­b mediated changes in BEC. HGF and its mimetic, 1K1, were able to prevent oxidative stress induced EMT in BEC. Furthermore 1K1 showed a smaller induction of autophagy than HGF and was able to prevent up regulation of senescence markers. The paradigm of oxidative stress-­induced senescence leading to EMT was assessed in the current study, with identification of powerful therapeutic agents able to prevent these changes. This suggests that premature cellular ageing (senescence) in acute liver disease could be pharmacologically prevented from occurring. Inhibition of senescence prevents disease promotion by the effects of the SASP, blocking the progression to chronic disease; this may well apply to all organ systems.
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Books on the topic "Biliary epithelium"

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Joplin, Ruth Elizabeth. Investigations into the role of intrahepatic biliary epithelial cells in primary biliary cirrhosis. Birmingham: University of Birmingham, 1991.

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Parola, Maurizio. Biochemical studies on biliary epithelial cells isolated from rat liver. Uxbridge: Brunel University, 1990.

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Keogh, Adrian Colin. Anti-mitochondrial antigen on human biliary epithelial cells [: A study of membrane expression of dihydrolipoamide acetyltransferase sub unit of pyruvate dehydrogenase on human biliary epithelial cells]. Birmingham: University of Birmingham, 2001.

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Gianfranco, Ph.D. Alpini (Editor), Domenico, M.D. Alvaro (Editor), Marco, M.D. Marzioni (Editor), Gene, M.D. LeSage (Editor), and Nicholas, M.D. LaRusso (Editor), eds. The Pathophysiology of Biliary Epithelia: Medical Intelligence Unit. Landes Bioscience, 2004.

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Alpini, Gianfranco. Pathophysiology of Biliary Epithelia. Taylor & Francis Group, 2020.

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Alpini, Gianfranco. Pathophysiology of Biliary Epithelia. Taylor & Francis Group, 2020.

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Alpini, Gianfranco. Pathophysiology of Biliary Epithelia. Taylor & Francis Group, 2020.

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Alpini, Gianfranco. Pathophysiology of Biliary Epithelia. Taylor & Francis Group, 2020.

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Keshav, Satish, and Palak Trivedi. Liver cancer. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0218.

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Primary hepatocellular carcinoma (HCC) arises from hepatocytes and is one of the commonest solid-organ malignancies in the world, particularly in the Far East and in sub-Saharan Africa. Cholangiocarcinoma arises from the biliary epithelium. The incidence is rising in the West, and primary sclerosing cholangitis (PSC) is an important risk factor (15% lifetime risk). Other forms of liver cancer include metastatic cancer, which is much more common in the West than any primary liver cancer, accounting for 90% of liver cancers and for which common primary sites are the colon, the stomach, the breasts, and the lungs; hepatoblastoma, which is an uncommon malignancy in children, originating from immature liver cell precursors; haemangiosarcomas, which are also rare, are malignant tumours arising from the blood vessels in the liver and can be very rapidly growing; and gall bladder cancer, arising from the gall bladder epithelium. Gallstones and PSC are risk factors for gall bladder cancer; in particular, PSC confers a risk >160 times that of the control population. This chapter primarily focuses on HCC.
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Biliary and pancreatic ductal epithelia: Pathobiology and pathophysiology. New York: M. Dekker, 1997.

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Book chapters on the topic "Biliary epithelium"

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Nieuwenhuis, E. A., J. J. G. H. M. Bergman, and R. E. Pouw. "Radiofrequency Ablation of Barrett’s Epithelium." In Gastrointestinal and Pancreatico-Biliary Diseases: Advanced Diagnostic and Therapeutic Endoscopy, 1–16. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-29964-4_6-1.

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Nieuwenhuis, E. A., J. J. G. H. M. Bergman, and R. E. Pouw. "Radiofrequency Ablation of Barrett’s Epithelium." In Gastrointestinal and Pancreatico-Biliary Diseases: Advanced Diagnostic and Therapeutic Endoscopy, 89–104. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-56993-8_6.

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Leclercq, Philippe, and Raf Bisschops. "Cryotherapy and Argon Ablation of Barrett’s Epithelium." In Gastrointestinal and Pancreatico-Biliary Diseases: Advanced Diagnostic and Therapeutic Endoscopy, 1–37. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-29964-4_7-1.

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Leclercq, Philippe, and Raf Bisschops. "Cryotherapy and Argon Ablation of Barrett’s Epithelium." In Gastrointestinal and Pancreatico-Biliary Diseases: Advanced Diagnostic and Therapeutic Endoscopy, 105–40. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-56993-8_7.

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D’Aldebert, E., M. J. Biyeyeme Bi Mve, M. Mergey, D. Wendum, A. Coilly, L. Fouassier, C. Corpechot, R. Poupon, C. Housset, and N. Chignard. "Bile salts control the antimicrobial peptide cathelicidin through nuclear receptors in the human biliary epithelium." In Bile Acid Biology and Therapeutic Actions, 86–94. Dordrecht: Springer Netherlands, 2009. http://dx.doi.org/10.1007/978-1-4020-9644-0_13.

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Saidman, S., B. Markus, A. J. Demetris, J. Fung, A. Zeevi, T. Starzl, and R. Duquesnoy. "Role of HLA Class II-Specific Alloreactive T Cells in Biliary Epithelium Injury Associated with Liver Transplant Rejection." In Immunobiology of HLA, 533–35. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_232.

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Mizuguchi, Yoshiaki, Susan Specht, Kumiko Isse, John G. Lunz, and Anthony J. Demetris. "Biliary Epithelial Cells." In Molecular Pathology Library, 27–51. Boston, MA: Springer US, 2010. http://dx.doi.org/10.1007/978-1-4419-7107-4_4.

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Leite, M. Fatima, Mateus T. Guerra, Viviane A. Andrade, and Michael H. Nathanson. "Signaling pathways in biliary epithelial cells." In Signaling Pathways in Liver Diseases, 15–33. Chichester, UK: John Wiley & Sons, Ltd, 2015. http://dx.doi.org/10.1002/9781118663387.ch2.

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Leite, M. Fatima, Viviane A. Andrade, and Michael H. Nathanson. "Signaling Pathways in Biliary Epithelial Cells." In Signaling Pathways in Liver Diseases, 25–39. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-00150-5_2.

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Rubio-Tomás, Teresa, Beatriz Aguilar-Bravo, and Pau Sancho-Bru. "Genetic Lineage Tracing of Biliary Epithelial Cells." In Methods in Molecular Biology, 45–57. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8961-4_5.

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Conference papers on the topic "Biliary epithelium"

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Lee, Yuyang, Ryo Sudo, Tomoya Komatsu, Norihisa Miki, Toshihiro Mitaka, Mariko Ikeda, and Kazuo Tanishita. "Microfluidic Hydrostatic Deposition Patterning for a confined hepatocyte-biliary epithelial cell co-culture system." In 2011 International Symposium on Micro-NanoMechatronics and Human Science (MHS). IEEE, 2011. http://dx.doi.org/10.1109/mhs.2011.6102148.

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Junger, H., S. Fichtner-Feigl, HJ Schlitt, Z. Laszik, and SM Brunner. "Induction of biliary epithelial wound healing and angiogenesis through IL6 in donor bile ducts after liver transplantation." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677133.

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Reich, M., L. Spomer, J. Höhne, J. Stindt, JR Hov, TH Karlsen, C. Schramm, et al. "TGR5 (Gpbar-1) expression is downregulated in biliary epithelial cells in livers of PSC patients and in Abcb4-/- mice." In 37. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1721944.

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Clapéron, Audrey, Martine Mergey, Nathalie Guedj, Blandine de Singly, Yves Chrétien, Valérie Paradis, Chantal Housset, and Laura Fouassier. "Abstract 5205: EBP50, a PDZ-containing protein, regulates EGFR-induced cell scattering and migration in human cancer biliary epithelial cells." In Proceedings: AACR 101st Annual Meeting 2010‐‐ Apr 17‐21, 2010; Washington, DC. American Association for Cancer Research, 2010. http://dx.doi.org/10.1158/1538-7445.am10-5205.

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