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1
Hellwig, Michael. "Proteolytische Freisetzung und epithelialer Transport von Maillard-Reaktionsprodukten und Crosslink-Aminosäuren." Doctoral thesis, Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-78234.
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Proteingebundene Maillard-Reaktionsprodukte (MRP) und Crosslink-Aminosäuren (CLAS) werden mit der Nahrung täglich in nicht unerheblichen Mengen aufgenommen. In Humanstudien wurde gezeigt, dass einzelne dieser Produkte resorbiert werden. Die Beteiligung einzelner MRP und CLAS an pathophysiologischen Prozessen wird diskutiert.
Im ersten Teil der Arbeit wurden MRP (Fructoselysin, Lactuloselysin, CML, CEL, Pyrralin, MG-H1, Pentosidin) und CLAS (LAL, Glutamyllysin) in Casein angereichert und die Caseine einer simulierten gastrointestinalen Verdauung unterzogen. Mit der posttranslationalen Modifizierung ging eine Verschlechterung der Verdaubarkeit einher. Dies zeigte sich daran, dass während der Verdauung bei zunehmendem Modifizierungsgrad Peptide mit Molmassen > 1000 Da schlechter abgebaut wurden und somit die Bildung von Peptiden < 1000 Da abnahm. Die Verschlechterung der Verdaubarkeit ließ sich vor allem auf die Quervernetzung der Caseine, weniger auf die Modifizierung von Aminosäuren zurückführen.
Zudem wurde die Freisetzbarkeit einzelner Aminosäuren durch posttranslationale Modifizierung gesenkt. Dies konnte praktisch ausschließlich auf die Modifizierung von Lysinresten, nicht auf die Quervernetzung, zurückgeführt werden. Vor allem Aminosäuren, die im Casein in der Nähe von Lysinresten überrepräsentiert sind, wurden mit zunehmender Modifizierung schlechter freigesetzt. Die modifizierten Aminosäuren selbst wiesen ein sehr differenziertes Freisetzungsmuster auf. Amadori-Produkte wurden sehr gut freigesetzt, quervernetzende Aminosäuren dagegen nur zu einem geringen Anteil.
Als Referenzsubstanzen für chromatographische Messungen und als Testsubstanzen für Inhibitions- und Transportexperimente wurden im zweiten Teil der Arbeit insgesamt 19 freie MRP (Fructoselysin, Lactuloselysin, Tagatoselysin, Ribuloselysin, Carboxymethyllysin, Carboxyethyllysin, Pyrralin, Formylin, Maltosin, MG-H1, 3-DG-H, PIO, Argpyrimidin, Pentosidin) und CLAS (Lysinoalanin, π- und τ-Histidinoalanin, Ornithinoalanin, Lanthionin) in hohen Ausbeuten synthetisiert und charakterisiert. Zwölf der Produkte (Fructoselysin, Carboxymethyllysin, Carboxyethyllysin, Pyrralin, Formylin, Maltosin, MG-H1, Argpyrimidin, Lysinoalanin, π- und τ-Histidino¬alanin und N-ε-(γ-Glutamyl)-Lysin) wurden erstmals auch Dipeptidderivate (Ala-Xaa bzw. Xaa-Ala) synthetisiert und charakterisiert.
Mithilfe von Kompetitionsexperimenten an Caco-2-Zellen konnte gezeigt werden, dass freie MRP und CLAS die Aufnahme von L-[3H]Lysin kaum hemmten und somit nicht mit Transportsystemen für basische Aminosäuren wechselwirken können. Der überwiegende Teil der dipeptidgebundenen Derivate hemmte jedoch in konzentrationsabhängiger Weise den Transport von [14C]Gly-Sar . Diese Dipeptide stellen somit z.T. hoch affine Inhibitoren des Peptidtransporters dar. Die Affinität zum Transporter ist stark sequenzabhängig.
Caco-2-Zellen, die als Monolayer wachsen, wurden auf porösen Polycarbonatmembranen kultiviert und zu Transportstudien eingesetzt. Keines der freien MRP und CLAS wurde aktiv über den Monolayer transportiert. Wurden die Derivate dagegen dipeptidgebunden eingesetzt, stieg, außer bei fructosylierten Peptiden, der transepitheliale Transport stark an. Allerdings wurden die Peptide meist nicht intakt transportiert, sondern intrazellulär gespalten und die freien Aminosäuren basolateral abgegeben. Zum Teil reicherten sich die modifizierten Aminosäuren, besonders die hydrophilen, intrazellulär an. Hydrophobe Aminosäuren (Pyrralin, Formylin, Maltosin, Argpyrimidin) konnten die Zelle dagegen schnell verlassen. Diese Aminosäuren sollten daher auch in vivo effektiv resorbiert werden.
In Kompetitionsexperimenten an OK-Zellen zeigte sich, dass modifizierte Aminosäuren auch an Nierenzellen nicht mit Transportsystemen für Lysin wechselwirken. Keine der freien Aminosäuren wurde aktiv über den OK-Zellmonolayer transportiert. Somit ist nicht von einer renalen Reabsorption der untersuchten MRP und CLAS auszugehen.
2
Zimmermann, Christian [Verfasser]. "Epithelialer Transport und immunologische Effekte von Gliadinpeptiden in vitro / Christian Zimmermann." Gießen : Universitätsbibliothek, 2014. http://d-nb.info/1068825634/34.
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Hellwig, Michael [Verfasser], Thomas [Akademischer Betreuer] Henle, and Sabine [Akademischer Betreuer] Kulling. "Proteolytische Freisetzung und epithelialer Transport von Maillard-Reaktionsprodukten und Crosslink-Aminosäuren / Michael Hellwig. Gutachter: Thomas Henle ; Sabine Kulling. Betreuer: Thomas Henle." Dresden : Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2011. http://d-nb.info/1067729429/34.
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Hille, Carsten. "Charakterisierung von Transportmechanismen in der Speicheldrüse der Schabe Periplaneta americana." Phd thesis, Universität Potsdam, 2006. http://opus.kobv.de/ubp/volltexte/2006/942/.
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Die Aktivierung der Speichelsekretion erfolgt in der innervierten Speicheldrüse der Schabe Periplaneta americana durch die biogenen Amine Dopamin (DA) und Serotonin (5-HT). Die Acini der Speicheldrüse sezernieren einen Primärspeichel, der in den Ausführgängen modifiziert wird. Die durch DA und 5-HT aktivierten Signalwege sowie die an der Elektrolyt- und Flüssigkeitssekretion bzw. Speichel-modifikation beteiligten Transportmechanismen sind weitgehend unbekannt.Mikrofluorometrische Ca2+-, Na+- und pH-Messungen in Kombination mit pharmakologischen Experimenten, biochemische Messungen der Aktivitäten von Ionentransport-ATPasen sowie videomikroskopische Analysen zu transepithelialen Wasserbewegungen wurden in dieser Arbeit durchgeführt. Sie sollten Informationen über die an der Speichelbildung und -modifikation beteiligten Transportmechanismen und die Signalwege liefern, welche durch DA und/oder 5-HT aktiviert werden.
Wesentliche Ergebnisse dieser Arbeit waren:
- Messungen des intrazellulären pH (pHi) in Gangzellen zeigten, dass isolierte Ausführgänge mit Acini bei Stimulierung mit DA und 5-HT stark ansäuerten. In isolierten Ausführgängen ohne Acini verursachte nur DA eine schwache Ansäuerung. Da nur die Ausführgänge dopaminerg innerviert sind, die Acini jedoch dopaminerg und serotonerg, zeigt dieses Ergebnis, dass die DA- und/oder 5-HT-induzierte Primärspeichelbildung die Ursache für die pHi-Änderungen in den Gangzellen ist. pHi-Messungen in den Gangzellen geben also auch Hinweise auf Transportvorgänge in den Acini.
- Der Na+-K+-2Cl--Symporter und der Cl--HCO3--Antiporter, gekoppelt mit dem Na+ H+-Antiporter (NHE) waren an der NaCl-Aufnahme in die peripheren Zellen der Acini zur Bildung des NaCl-reichen Primärspeichels beteiligt. Die Aktivität dieser Transporter hing von der CO2/HCO3--Verfügbarkeit ab und war Ca2+-abhängig.
- Die starke Ansäuerung in den Gangzellen hing nicht von der Aktivität der apikalen vakuolären Protonen-ATPase (V-H+-ATPase), aber von der Aktivität der basolateralen Na+-K+-ATPase ab, die anscheinend in den Ausführgängen die Speichelmodifikation energetisiert.
- In isolierten Ausführgängen mit Acini waren die V-H+-ATPase und Na+-abhängige Transporter (u. a. NHE) an der Erholung von einer DA-induzierten oder einer NH4Cl-Vorpuls-induzierten Ansäuerung in den Gangzellen beteiligt. Bei der Regulation des pHi in unstimulierten Gangzellen spielten diese Transporter keine Rolle.
- In isolierten Ausführgängen mit Acini induzierte DA in den Gangzellen einen Anstieg der [Na+]i und, zeitlich verzögert, auch der [Ca2+]i. Der [Na+]i-Anstieg war von der Aktivität der Acini abhängig und erfolgte möglicherweise über apikale Na+-Kanäle. Der [Ca2+]i-Anstieg war graduiert und tonisch. Der DA-induzierte [Na+]i-Anstieg in den Gangzellen und deren Depolarisation führten dazu, dass der basolaterale Na+-Ca2+-Antiporter in den Ca2+-Influx-Modus umkehrte. Die daraus resultierende tonische [Ca2+]i-Erhöhung könnte an der Regulation der Na+-Rückresorption beteiligt sein.
- Zum Nachweis transepithelialer Flüssigkeitsbewegungen in isolierten Ausführgängen wurde eine videomikroskopische Methode entwickelt. Isolierte Ausführgänge ohne Acini resorbierten im unstimulierten Zustand Flüssigkeit aus dem Ausführganglumen. Möglicherweise sezernieren die Acini auch im unstimulierten Zustand mit geringerer Rate einen Primärspeichel, der in den Ausführgängen resorbiert wird. Die Resorption war ATP-abhängig. Der ATP-verbrauchende Transportmechanismus konnte nicht identifiziert werden. Weder die Na+-K+-ATPase noch die V-H+-ATPase waren an der Resorption beteiligt.
Diese Arbeit trug zur Kenntnis der komplexen Funktionsweise von Speicheldrüsen in Insekten bei und erweiterte das lückenhafte Wissen über die zellulären Wirkungen biogener Amine in Insekten. Zudem wurden in dieser Arbeit viele Parallelen zu Funktionsweisen der Speicheldrüsen in Vertebraten deutlich.
The acinar salivary glands in the cockroach Periplaneta americana are innervated by dopaminergic and serotonergic fibers and secrete a NaCl-rich primary saliva upon stimulation with the biogenic amines dopamine (DA) or serotonin (5-HT). The ducts downstream of the acini are thought to modify the primary saliva by Na+ reabsorption and K+ secretion. The electrolyte and fluid transport processes activated by DA and 5-HT as well as the second messenger pathways mediating between the biogenic amine receptors and the effector transport mechanisms are poorly understood.In this sudy, microfluorometrical Ca2+, Na+ and pH measurements were performed in combination with pharmacological experiments. Furthermore, ATPase activity assays and microscopical analyses of transepithelial fluid transport were done. The aim of this work has been the characterisation of the DA-induced transport mechanisms in the cockroach salivary glands in order to improve our understanding of the cellular actions of biogenic amines in insects.
Intracellular pH measurements in duct cells of isolated small lobes of salivary glands consiting of several acini and ducts showed a strong intracellular acidification upon DA or 5-HT stimulation. On the other hand, only a small intracellular acidification could be recognised in isolated ducts without acini. The acini are innervated by dopaminergic and serotonergic fibers, whereas the ducts are innervated only by dopaminergic fibers. Thus, this result demonstrates, that the DA- or 5-HT-induced production of primary saliva in the acini causes the intracellular pH changes in the ducts. Consequently, intracellular pH measurements in ducts are also useful to characterise transport processes in the acini.
The Na+-K+-2Cl- cotransport and/or the Cl--HCO3- exchange combined with the Na+ H+ exchange (NHE) were responsible for the NaCl uptake at the basolateral membrane in the peripheral cells of the acini during production of primary saliva. The activity of these transporters was regulated by the CO2/HCO3--availability and was Ca2+-dependent. The activity of the basolateral Na+-K+-ATPase, but not of the apical vacuolar-type proton pump (V-H+-ATPase) in the duct cells was necessary for the strong intracellular acidification in the ducts with acini. Thus, the Na+-K+-ATPase seems to energise the saliva modification in the ducts. In ducts with acini, the V-H+-ATPase and Na+-dependent transporters (e.g. NHE) were responsible for the pH-recovery after a DA- or NH4Cl-induced intracellular acidification in the duct cells. In the regulation of the intracellular resting pH these transporters played a minor role. In addition, DA induced an increase in the intracellular Na+ concentration, followed by an increase in the intracellular Ca2+ concentration in duct cells with acini, but never in duct cells without acini. The Na+ elevation was probably the result of the activity of apical Na+ channels. The DA-induced Na+ elevation and a depolarisation of the basolateral membrane of the duct cells reversed a Na+-Ca2+ exchange activity into the reverse mode causing a graded Ca2+ elevation in duct cells. The Ca2+ elevation is probably involved in the regulation of the Na+ reabsorption during saliva modification. Transepithelial fluid transport in isolated ducts was detected with a fluorescent microscopical method. Already unstimulated isolated ducts reabsorbed fluid from the duct lumen to the bath side. Perhaps unstimulated acini possess a basic secretion rate and this primary saliva is than reabsorbed in the ducts. The fluid reabsorption was ATP-dependent, but the ATP-consuming transport mechanism could not be identified. Neither the basolateral Na+-K+-ATPase, nor the apical V-H+-ATPase were involved in fluid reabsorption. This work extends our knowledge about the complex function of insect salivary glands and about the cellular action of biogenic amines in insects. Additionally, it indicates lots of similarities between the functions of salivary glands in vertebrates and invertebrates.
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Kaltofen, Till. "Geschlechtsspezifische Unterschiede im fetalen alveolaren Natriumtransport." Doctoral thesis, Universitätsbibliothek Leipzig, 2017. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-218692.
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Die Inzidenz des Atemnotsyndroms ist bei männlichen Neugeborenen etwa 1,7-mal so hoch wie bei weiblichen. Zur Erforschung der Ursachen dieser Tatsache wurden in der vorliegenden Arbeit geschlechtsabhängige Unterschiede im transepithelialen Natriumtransport an fetalen distalen Lungenepithelzellen von Ratten untersucht. Die zugrunde liegende Versuchsanordnung stellt ein Modell der Typ II Pneumozyten des späten Frühgeborenen dar. In Ussing Kammer Messungen wurde ein höherer Natriumtransport in weiblichen Zellen im Vergleich zu männlichen Zellen nachgewiesen. Des Weiteren zeigten Genexpressionsanalysen eine höhere Expression der am Natriumtransport beteiligten Kanäle und Transporter in weiblichen Zellen. Um mögliche Ursachen der festgestellten Geschlechtsunterschiede zu eruieren, wurde die Genexpression von Hormonrezeptoren untersucht. Die Ergebnisse lassen vermuten, dass die Rezeptoren weiblicher Geschlechtshormone dabei eine wichtige Rolle spielen. Abschließend betrachtet diese Arbeit die absolute Zahl fetaler distaler Lungenepithelzellen in Rattenfeten beider Geschlechter. Hierbei fanden sich ebenfalls Geschlechtsdifferenzen.
Zusammenfassend kann die vorliegende Arbeit zu einem besseren Verständnis der Pathogenese und der Inzidenz des Atemnotsyndroms des Frühgeborenen beitragen.
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Helwig, Maren. "Transport von HIV-1 durch epitheliale Zellen." Doctoral thesis, Humboldt-Universität zu Berlin, Mathematisch-Naturwissenschaftliche Fakultät I, 2007. http://dx.doi.org/10.18452/15613.
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Als ein Grund für die vertikale Transmission von HIV von der Mutter auf das Kind während der Schwangerschaft bzw. der Geburt wird der Transport von HIV durch die Eihaut diskutiert. Hierbei handelt es sich wahrscheinlich um einen rezeptorvermittelten Transport, der auf einer Interaktion zwischen einer Lektin-bindenden Domäne auf dem viralen Oberflächenglykoprotein gp120 und einem Rezeptor auf der epithelialen Oberfläche beruht. In der vorliegenden Arbeit konnte die in den Transport von zellfreien HIV-1 durch epitheliale Zellen beteiligte Domäne auf gp120 erstmals näher charakterisiert werden. Überlappende Oligopeptide –basierend auf der Aminosäurensequenz von gp120– wurden zur Hemmung der Transzytose von HIV-1 durch humane Amnionzellen verwendet. Vier dieser Oligopeptide inhibierten die Transzytose von HIV-1 signifikant. Ein synthetisches Peptid (Env362-420) mit einer Länge von 59 Aminosäuren, welches die Sequenz der inhibierenden Oligopeptide darstellt, reduzierte die Menge an transportierten Viren ebenfalls, unabhängig vom HIV-1 Subtyp. Im Weiteren konnte der Transport von HIV-1 durch polyklonale Antikörper in Seren HIV-Infizierter, die mit Env362-420 reagierten, und durch Seren, die durch eine Immunisierung von Kaninchen mit Env362-420 gewonnen wurden, inhibiert werden. Antikörper gegen die in den Transport involvierte Domäne konnte in Seren HIV-Infizierter zu jedem Stadium der Infektion nachgewiesen werden. Bei einer Expression der Antikörper in der frühen Infektionsphase wäre ein positiver Einfluss auf die Prognose der Krankheit vorstellbar. Ob ein Zusammenhang zwischen einer Antikörperexpression gegen Env362-420 in HIV-infizierten Schwangeren und der Wahrscheinlichkeit einer HIV-Transmission auf das Kind besteht, muss noch geklärt werden. Env362-420 kann zur Identifizierung des Rezeptors auf der epithelialen Oberfläche, welcher in die Transzytose von HIV involviert ist, und zur Entwicklung von Inhibitoren der Mutter–Kind-Übertragung von HIV herangezogen werden.The transport of HIV through the fetal membranes is discussed as one possible reason for the vertical transmission of HIV from mother to child during pregnancy or labor. HIV can penetrate epithelial barriers by a receptor-mediated transport mechanism involving interaction of a lectin-like domain on the viral glycoprotein gp120 and a receptor on the epithelial surface. In this study the domain on gp120 involved in transcytosis of cell-free HIV-1 through epithelial cells was characterized in more detail. Overlapping oligopeptides of gp120 were used to inhibit transcytosis of HIV 1 through an amnion cell monolayer. Four oligopeptides significantly inhibited transcytosis of HIV 1. A synthetic oligopeptide (Env362-420) with a length of 59 amino acids representing the sequence of the four inhibiting oligopeptides significantly reduced the transport of HIV, independent of the HIV 1 subtype. Furthermore, human HIV-positive sera with antibodies reacting with the domain Env362-420 and rabbit sera raised against the oligopeptide Env362-420 also inhibited the transport of HIV-1. Antibodies directed against the transcytosis domain could be detected in sera from every stage of infection. The development of these antibodies in the early stage of infection might play a role in the outcome of the HIV disease.It has to be investigated whether HIV 1-infected women who developed these antibodies show a lower rate of HIV transmission to their offspring than those without such antibodies. Env362–420 can also be used as a tool to identify the receptor involved in transcytosis on the epithelial cell surface and to develop inhibitors that could help prevent mother-to-child transmission of HIV during pregnancy or labor.
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Johnson, Deborah. "Regulation of iron transport and transporter expression in intestinal epithelial cells by dietary and humoral agents." Thesis, University of Surrey, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.426040.
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Pickles, Raymond J. "Intracellular calcium ions in epithelial ion transport." Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307103.
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Bradford, Emily M. "Epithelial Ion Transport and Gastrointestinal Fluid Homeostasis." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1265985361.
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Collares, Buzato Carla Beatriz. "Modulation of paracellular permeability and intercellular junctions in cultured epithelia." Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283019.
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Geada, Maria do Rosario Moreno Cruz Colaco. "Molecular mechanism of magnesium transport in epithelial cells." Thesis, University of Central Lancashire, 1998. http://clok.uclan.ac.uk/20300/.
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Gastrointestinal secretions are controlled mainly by the gut hormones and by the neurotransmitters released by the autonomic nervous system. The hormones and neurotransmitters (secretagogues) utilise different intracellular mediators to elicit enzyme and fluid secretion. One particular mediator is the second messenger calcium (Ca2+) and there is now much evidence that the abundant divalent cation magnesium (Mg 25 may play an important physiological role in regulating the mobilisation of cellular Ca 2t Thus, the present study was designed to investigate (a) the effect of a modification of extracellular Mg2 on secretagogue-evoked enzyme and hydrochloric acid (HCI) secretion and Ca 2 homeostasis in the pancreatic acinar cells and parietal cells and (b) to characterise the molecular mechanism of Mg 2 transport using fluorimetric and spectroscopic studies. The results have shown that application of either cholecystokinin-octapeptide (CCK-8) or acetylcholine (ACh) to rat pancreatic segments can result in marked increases in amylase and trypsinogen output in normal (1.1 mlvi) extracellular magnesium [Mg 2 0. When [Mg2 0 was elevated to 10 mlvi, there was a significant (P C 0.05) decrease in secretagogue-evoked pancreatic enzyme secretion. On the other hand, in low (0 mM) [Mg2 0 both CCK-8 and ACh elicited marked increases in enzyme secretion similar to the responses obtained in the presence of normal [Mg 2 o . The effects closely correlate with the concurrent reductions and increases in intracellular free calcium concentrations 2 +-. [Ca j ifrom studies performed with fljra-2-AM loaded pancreatic acmi dunng perturbation of [Mg2 0 These findings indicate that Mg 24 can influence enzyme secretion by regulating Ca24 mobilisation. The possible site of action of Mg2 in controlling Ca24 appears to be at the level of Ca 24 influx, since experiments, using thapsigargin or ionomycin, agents which release Ca2+ from intracellular Ca2+ stores, were not affected by a variation in [Mg 2 0 . This study also employed the technique of microspectrofluoritnetry to fi.irther characterise the mechanism of Mg2 transport using mouse pancreatic acinar cells loaded with magfisra-2-AM. Stimulation of acini with CCK-8 evoked an initial sharp rise in [Mg 2 1 followed by a decrease to a new steady-state level (Mg 24 efflux). On removal of CCK-8 [Mg2 1 returned to the pre-stimulated basal level (Mg 24 reuptake). In contrast, CCK-8 gave rise to Ca24 oscillations. When acinar cells were co-loaded with 1 ,2-bis (2- aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA) (10 piM) and either magflira-2-AM or fijra-2-AM, CCK-8 evoked only the normal decrease in [Mg 2 j and a slight [Ca2 j+ ,e levation. (10 nM). This . results suggests that the in. i.t ial ns. e in. [Mg 2+-. ji seen with CCK-8 in normal conditions may be due to the Ca 24 interfering with the magfura-2-AM signal. Both thapsigargin (0.5 pM) and ionomycin (5 piM) evoked a marked decrease in [Mg 2+,. . . . 2-i-,jj in magfiira-2-AM loaded acmar cells and an elevation in [Ca j' from fi.ira-2- VAM loaded acinar cells. The results indicate that cytosolic Ca 2 is associated with secretagogue-induced decrease in [Mg 24]1. When acinar cells were pre-treated with either forskolin (10 pM), N Nitro-L-arginine (N-NLA; 2 mM), 8 -Bromo guanosine guanosine cyclic mono-phosphate (Br cGMP; 100 pM) or staurosporine (1 pM), CCK-8 elicited only a small decrease in [Mg24]j compared to a much larger response with CCK-8 alone. In contrast, genistein (10 pM) and 12-0-tetradecanoyl phorbol 13 a acetate (TPA; 1 pM) augmented the decrease in [Mg 24]1 evoked by CCK-8. The results indicate that Ca2 mobilising secretagogues can stimulate Mg 2 efflux which is also mediated by a number of intracellular mediators. This study also investigated the mechanism of Mg 2 transport from the rat pancreas. Permeabilised pancreatic acini were loaded with Mg 2 ' by employing a high Mg2 (12 mM) buffer containing the tonophore A23 187 (6 .dv1). Net Mg 2+ efflux was measured by using the technique of atomic absorption spectrophotometry. Incubation of pre-loaded acini in a buffer deficient in Mg2 resulted in a large and time-dependent release of Mg 2 with maximal efflux occuning within 40 min. Pre-treatment of loaded acini with either bumetadine, SITS or ouabain had no significant effect on Mg2 efflux. In contrast, when acini were pre-treated with either 10 mM dinitrophenol (DNP), io M amiloride, 1 mM lidocaine or I mM quinidine there were significant (P < 0.05) decreases in net Mg 2 efflux. Replacement of extracellular sodium [Na4]0 with either N -methyl-D-glucamine (NMDCI), or choline chloride resulted in a significant (P C 0.05) inhibition of Mg2 effiux. The results of this study indicate that Mg 2 transport (efflux) in rat pancreatic acinar cells may not be associated with the N atKtATPase, the NatKtCl cotransporter or the anion exchanger, but with a Na+ -sensitive Mg2+ transport system. However, this Na+ sensitivity was found to be species dependent as in mouse pancreatic acinar cells Mg2 transport occurred in the absence of [NC] 0 . Studies performed on rat gastric panetal cells have demonstrated that elevated [Mg 2 10 has the same inhibitory effects on secretagogue-evoked acid secretion and cellular Ca 2 transport as that observed with pancreatic acinar cells whereas low [Mg 2 0 had the opposite effect. In conclusion, the results of this study have demonstrated marked interactions between the two divalent cations Mg2 and Ca2 in epithelial secretory cells of the gastrointestinal tract. Mg2+ seems to regulate secretagogue-evoked secretion by controlling cellular Ca2+ mobilisation.
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Beltinger, Johannes Hermann. "Studies on colonic epithelial ion transport and barrier function." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311747.
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Armstrong, Gillian. "Solute transport and intracellular pH in intestinal epithelial cells." Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320390.
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Rexhepaj, Rexhep. "The role of serine-threonine-kinases in epithelial transport." [S.l. : s.n.], 2008.
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Jensen, Barbara Ann. "The effects of calcineurin inhibitors on epithelial electrolyte transport." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10050573/.
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Calcineurin inhibitor (CNI)-induced hypertension is common after renal transplantation, rendering patients susceptible to cardiovascular and kidney disease, graft failure and death. CNI-induced hypertension occurs as a result of enhanced sodium retention by activation, via phosphorylation, of the renal thiazide-sensitive NaCl cotransporter, NCC (SLC12A3). CNI-treated renal transplant patients also have increased NCC abundance in isolated urinary exosomes. The studies described in this thesis were designed to investigate the effects of CNI treatment on mouse renal and intestinal sodium transport proteins, to determine whether alterations in proteins other than NCC may also contribute towards sodium retention. These changes were compared with those in an established mouse model of metabolic syndrome, comprising hypertension, insulin resistance, obesity and hypercholesterolemia which are also associated with CNI use. The abundance of NCC and phospho-NCC was also investigated in urinary exosomes from patients taking CNIs or with Gitelman syndrome. There was a higher abundance of NCC and pNCC in urinary exosomes from CNI-treated renal transplant patients compared with patients with Gitelman syndrome. Both CNI-treated and metabolic syndrome rodent models displayed a significant increase in pNCC. No differences were observed for intestinal transport proteins with CNI-treatment, however, a lower abundance of PiT1 and SGLT1 in the small intestine was observed with high-fat feeding. Renal NHE3 and ENaC were down-regulated in CNI-treated mice, a response that could be compensatory to the upregulation of pNCC in the DCT. These data provide evidence that CNIs influence a number of renal sodium transport proteins that may contribute towards the development of hypertension following transplantation. These studies suggest an important role for calcineurin in the regulation of blood pressure and sodium transport in the kidney, and its possible involvement in the pathogenesis of hypertension and electrolyte disorders.
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Leibfried, Andrea. "Polarized transport of DE-Cadherin in Drosophila epithelial cells." Paris 6, 2009. http://www.theses.fr/2009PA066187.
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Le réseau des jonctions reliant les cellules entre-elles, les jonctions adhérentes (AJ), est nécessaire pour la fonction et la morphologie de l’épithélium. La stabilité et plasticité des AJ repose sur l’exocytose et l’endocytose de la protéine E-Cadhérine (E-Cad). Ma thèse montre que la perte de fonction des protéines Cdc42, Par-6 ou aPKC s’accompagne d’une accumulation apicale de structures intracellulaires d’E-Cad et d’une perturbation des AJ dans les cellules épithéliales de drosophile. Les structures ponctuelles proviennent de vésicules élargies et malformées qui émanent des AJ. Nous montrons que la protéine Cip4 est un effecteur de Cdc42 qui interagit avec la Dynamine et WASp (activateur d’Arp2/3). En conséquence, la perte de fonction des protéines Cip4, WASp ou Arp2/3 aboutit également à un défaut de l’endocytose de l’E-Cad. Cip4 et WASp agissent donc comme un lien entre Cdc42/Par-6/aPKC et le mécanisme d’endocytose précoce pour réguler l’endocytose de l’ E-Cad dans l’épithélium
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ZLATKINE, PHILIPPE. "Polarisation des cellules epitheliales renales transport de choline et synthese de phosphatidylcholine." Paris 7, 1994. http://www.theses.fr/1994PA077112.
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Une caracteristique de la structure des cellules epitheliales renales est la distribution polarisee des lipides entre le domaine apical et basolateral de la membrane plasmique. La presente etude a consiste a determiner les relations existant entre la polarisation des cellules mdck, la distribution du transport de choline et la synthese de phosphatidylcholine (pc). Une double approche basee sur l'utilisation d'une proteine specifique de transfert de la pc, et sur l'etude des etapes de la voie de biosynthese de ce phospholipide nous a permis de mettre en evidence: 1) la possibilite de changer une partie de la pc membranaire grace a une proteine specifique de transfert. L'utilisation d'une telle proteine a montre que le feuillet externe de la membrane apicale des cellules mdck contient au moins 5 a 8% de pc. 2) la presence d'un systeme de transport specifique de la choline dans les cellules mdck, caracterise par un km de 43 m et un vmax de 284 pmol/mg prot/5 min. Le transporteur est independant de la presence de sodium, il est inhibe par la carence en atp, l'addition de kcl ou la presence d'un inhibiteur specifique, l'hemicholinium-3. La distribution de ce systeme de transport est polarisee. Il est preferentiellement localise et/ou actif au pole basolateral des cellules cultivees sur support poreux. 3) une relation etroite entre le transport de choline et la voie de biosynthese de pc. La synthese de pc transite par la voie de la cdp, elle est polarisee et depend preferentiellement de l'entree basolaterale de choline pour les cellules cultivees sur filtre. Nos resultats suggerent fortement la presence d'un channeling polarise pour la synthese de pc dans les cellules mdck
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Bell, Cindy Lea. "Transport studies in primary cultures of mouse renal epithelial cells." Thesis, McGill University, 1986. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=75363.
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The Hyp (hypophosphatemic) mouse, a murine homologue of X-linked hypophosphatemia (XLH) in man, is a Mendelian disorder of phosphate (Pi) homeostasis. The mutant genotype is characterized by abnormal Pi transport at the brush border membrane (BBM) of the proximal tubule and a defect in renal metabolism of vitamin D$ sb3$. The exact nature of these defects has not been elucidated.In order to determine if the defect is intrinsic to the renal cell or dependent upon an extrinsic humoral factor, I established primary cultures of renal epithelial cells from normal and Hyp mouse kidney. The cultures demonstrated several differentiated properties of epithelial cells of the renal proximal tubule, the site of the Pi transport defect in the Hyp mouse.
Primary cultures initiated from Hyp mice had decreased Pi transport (expressed as an uptake ratio, Pi/$ alpha$-MG), and increased production of 24,25 dihydroxyvitamin D$ sb3$. These results provide evidence for the intrinsic nature of the primary defect in the Hyp mouse.
This appears to be the first time that expression of a mutant transport gene has been demonstrated in cultured renal cells.
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Kingseigh-Smith, Diarmuid James. "Effects of asthma prophylaxis agents on airway epithelial chloride transport." Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300507.
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O'Donoghue, D. L. "Quantitative analysis of ion transport in human airway epithelial cells." Thesis, University College London (University of London), 2014. http://discovery.ucl.ac.uk/1436428/.
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In the human airways, transepithelial ion transport is facilitated by a complex arrangement of ion channel, pump, cotransporter and tight junction proteins. The transepithelial potential difference (Vt), which shows characteristic changes in cystic fibrosis (CF) disease, is commonly measured in the study of epithelial ion transport. In this thesis I develop a mathematical model of ion transport in human nasal epithelia (HNE), in order to quantitatively investigate the relationship between individual transport protein activities and the transepithelial potential generated. In the first part of this work, I investigate the biophysical basis of hyperpolarised basal Vt and increased amiloride sensitive Vt in CF HNE cells. Using published electrophysiological measurements from in vitro experiments, I estimate the value of apical Na+ and apical Cl- permeability in both CF and non-CF HNE cells. I find apical Na+ permeability is increased in CF relative to non-CF cells, and apical Cl- permeability is decreased in CF, suggesting increased epithelial sodium channel (ENaC) activity, as well as decreased activity of anion specific CFTR channels, is responsible for the abnormal bioelectric properties of CF HNE cells. In the second part of this work, I focus on the nasal potential difference (NPD) test commonly made in patients with CF, investigating the biophysical basis of interpatient variability in NPD measurements. I find that the variation in amiloride insensitive Vt observed in a group of CF patients, cannot be accounted for by variation in apical Na+ and Cl- permeability alone. It is necessary to assume incomplete block of ENaC channels by amiloride, and patient to patient variability in other physiological parameters, in order to fully explain the observed variability in this cohort of NPD traces.
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Reiland, Joanne Elizabeth Donovan Maureen D. "Analysis of cell culture models of mammary drug transport." Iowa City : University of Iowa, 2009. http://ir.uiowa.edu/etd/316.
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Barrett, Martin Andrew. "Transport of cephalosporins across monolayers of some human epithelial cell lines." Thesis, King's College London (University of London), 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.300009.
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Sterling, Tremaine M. "Hormone Mediated Transport of Calcium and Phosphate in Polarized Epithelial Cells." DigitalCommons@USU, 2004. https://digitalcommons.usu.edu/etd/5544.
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The effects of 1,25(OH)2D3, PTH and 25(OH)D3 on phosphate or calcium uptake were studied in cultured, adherent chick enterocytes over a period of 10 min after hormone addition. Time course studies of cells treated with 130 pM 1,25(OH)2D3 showed an increase in 32P uptake as early as 3 min. Similar studies with 65 pM bPTH(l1-34) resulted in an increase in 45Ca uptake only if the cells had been cultured in serum. (OH)D3, which is not firmly established as an active metabolite of vitamin D, was shown to increase 45Ca uptake within 5 min at a 100 nM concentration.
Analyses of signal transduction events involving each hormone were undertaken using PKC and PKA inhibitors, chelerythrine and Rp-cAMP, respectively. In the presence of PKC inhibitor and 1,25(OH)2D3 elevated 32P levels were apparent; however, further investigations involving efflux studies showed PKC inhibition of 32P extrusion in the presence or absence of hormone. On the other hand, suppression of the PKA pathway stimulated an increase in 1,25(OH)2D3-mediated 32P uptake. Preincubation of enterocytes with Ab099 against a putative membrane receptor for 1,25(OH)2D3 abolished steroid-stimulated 32P uptake.
While PKC inhibition had no effect on 45Ca uptake in enterocytes exposed to 65 pM bPTH(1-34) in serum, pretreatment with PKA inhibitor resulted in 45Ca levels relatively close to basal levels. Cells pretreated with PKC inhibitor and exposed to 25(OH)D3 demonstrated no changes in 45Ca levels, whereas inhibition of PKA induced decreased 45Ca levels after 10 min of incubation.
In equivalent time course studies of membrane trafficking using confocal microscopy, potential vectorial transport initiated by each hormone was analyzed with agonist alone or in the presence of PKC and PKA inhibitors. In addition 1,25(OH)2D3 was tested in the presence of Ab099 against its putative membrane receptor. Visualization of these experiments using the endocytotic marker dye, FM 1-43, demonstrated that hormone-mediated membrane trafficking is rapid enough to contribute to ion transport. These results also suggest that vectorial vesicular transport mechanisms were involved to some extent in response to each hormone. Moreover, the pattern for membrane trafficking was different for each agonist.
These combined results indicate that adherent chick enterocytes demonstrate hormone-mediated uptake that occurs more rapidly than cells in suspension or in perfusion studies. This research supports previous studies that identify 25(OH)D3 as an active vitamin D metabolite. The PKA signal transduction pathway is a possible mechanism for PTH- and 25(OH)D3-mediated increases in 45Ca. In addition, a central role for the basal lateral membrane receptor protein, 1,25(OH)2D3MARRS-bp, in 1,25(OH)2D3-mediated 32P uptake is supported. Confocal imaging suggests that the transport mechanism for phosphate or calcium ions in the presence of these hormones involves vesicular carriers.
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Reancharoen, Tharnkamol. "Ion transporting activities of an epithelial cell line, HCA-7 colony 30." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.338258.
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Beattie, Lorraine Anne. "Electrophysiological analysis of the epithelial H+/oligopeptide transporter, PepT1." Thesis, University of Oxford, 2001. http://ora.ox.ac.uk/objects/uuid:2213d293-14cd-483b-88ab-7395e5c39b0c.
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The characteristics of transport by the epithelial, proton-coupled oligopeptide transporter, PepT1, have been investigated in PepT1 expressing Xenopus laevis oocytes using electrophysiological techniques. Membrane depolarisations and inward currents have been measured in response to various dipeptide substrates, including structurally modified and charged peptides. The latter part of this study has focussed on the role of phorbol esters on the regulation of PepT1-mediated peptide transport. I have shown that transport of neutral peptides is dependent on both pH and membrane potential. In addition, the carboxyl terminus plays an important role in substrate recognition and binding, as when blocked, the affinity of the substrate is reduced 10-fold. The importance of position of charge within a dipeptide on substrate binding has also been investigated using dipeptides where the charged amino acid residue is present at either the amino or carboxyl terminus. The results showed that the apparent order of affinity reversed upon extracellular acidification, thus charged residues within the peptide play an important role in substrate binding. The acute regulation of the oligopeptide transporter has been examined by studying the effects of phorbol esters on the transport of a neutral peptide, Gly-Gln. The active ester, PMA, was shown to decrease both the Ka and the Imax. Immunocytochemical studies have confirmed the electrophysiological findings.
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MORDRELLE, AGNES. "Contribution a l'etude du transport de l'acide l-glutamique dans la cellule epitheliale intestinale." Paris 11, 1998. http://www.theses.fr/1998PA112204.
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Present en grande quantite dans les proteines alimentaires, l'acide l-glutamique est un carrefour metabolique et un substrat energetique important pour la cellule epitheliale intestinale. De nombreuses questions demeurent quant a son mecanisme d'absorption par l'epithelium intestinal : l'intervention d'un systeme de transport de faible affinite au cote d'un systeme de forte affinite specifique des acides amines anioniques est l'objet d'une controverse et la distribution des systeme de transport le long de l'axe crypto-villositaire est encore completement inconnue. Les lignees epitheliales intestinales en culture ont ete largement utilisees pour l'etude des mecanisme de transport des nutriments et de leur regulation. Le transport de l'acide l-glutamique a ete etudie dans la lignee epitheliale intestinale indifferenciee de rat iec-17 et la lignee epitheliale intestinale d'origine humaine caco-2. La captation de l'acide l-glutamique dans la premiere lignee fait intervenir le systeme de transport na#+-independant x#-#c, ainsi que les systemes na#+-dependants de basse et haute affinite asc et x#a#,# #g#-. Ce dernier ne joue qu'un role modeste dans la capacite de transport de ces cellules vis-a-vis de l'acide l-glutamique. Le systeme de transport epithelial b#0, decrit comme etant susceptible de transporter egalement cet acide amine ne semble pas etre present dans cette lignee. Le transport de l'acide l-glutamique dans la lignee d'origine cancereuse colique caco-2 ne fait intervenir que la composante na#+-dependante de haute affinite x##a#,# #g. Dans ces cellules, nous avons, en utilisant la technique de protection a la rnase, observe la presence du transporteur de l'acide l-glutamique eaat1 et montre que le transporteur eaat3 decrit comme etant present dans l'intestin grele est quasiment indetectable. La differenciation des cellules caco-2 en cellules de type enterocytaire s'accompagne d'une augmentation significative de la capacite de transport de l'acide l-glutamique ainsi que d'une augmentation de la quantite d'arn messagers codant pour la proteine eaat1, suggerant une regulation transcriptionnelle du transport de l'acide l-glutamique. En conclusion, nous avons mis en evidence l'implication de differents mecanismes de captation de l'acide l-glutamique suivant le modele cellulaire utilise, ainsi qu'une regulation du transport de cet amine au cours de la differenciation enterocytaire de la lignee caco-2.
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Dickie, A. John. "Mechanisms by which endotoxin-stimulated alveolar macrophages impair lung epithelial sodium transport." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0025/MQ51593.pdf.
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Takayama, Akira. "Transport of cyclosporin A in kidney epithelial cell line (LLC-PK[1])." Kyoto University, 1995. http://hdl.handle.net/2433/160728.
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本文データは平成22年度国立国会図書館の学位論文(博士)のデジタル化実施により作成された画像ファイルを基にpdf変換したものであるKyoto University (京都大学)
0048
新制・論文博士
博士(医学)
乙第8919号
論医博第1514号
新制||医||613(附属図書館)
UT51-95-P410
(主査)教授 藤田 潤, 教授 吉田 修, 教授 乾 賢一
学位規則第4条第2項該当
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Panitsas, Konstantinos-Emmanuil. "Functional expression of the mammalian epithelial peptide transporter PEPT1." Thesis, University of Oxford, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.422669.
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Tavelin, Staffan. "New Approaches to Studies of Paracellular Drug Transport in Intestinal Epithelial Cell Monolayers." Doctoral thesis, Uppsala University, Department of Pharmacy, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3388.
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Studies of intestinal drug permeability have traditionally been performed in the colon-derived Caco-2 cell model. However, the permeability of these cell monolayers resembles that of the colon rather than that of the small intestine, which is the major site of drug absorption following oral administration. One aim of this thesis was therefore to develop a new cell culture model that mimics the permeability of the small intestine. 2/4/A1 cells are conditionally immortalized with a temperature sensitive mutant of SV40T. These cells proliferate and form multilayers at 33°C. At cultivation temperatures of 37 – 39°C, they stop proliferating and form monolayers. 2/4/A1 cells cultivated on permeable supports expressed functional tight junctions. The barrier properties of the tight junctions such as transepithelial electrical resistance and permeability to hydrophilic markers resembled those of the human small intestine in vivo. These cells lacked functional expression of drug transport proteins and can therefore be used as a model to study passive drug permeability unbiased by active transport. The permeability to diverse sets of drugs in 2/4/A1 was comparable to that of the human jejunum for both incompletely and completely absorbed drugs, and the prediction of human intestinal permeability was better in 2/4/A1 than in Caco-2 for incompletely absorbed drugs. The small intestinal-like paracellular permeability of 2/4/A1 thus enables better predictions of drug permeability in the small intestine than does Caco-2.
The studies of the paracellular route and its importance for intestinal drug permeability was also in focus in the second part of this thesis, in which a new principle for tight junction modulation was developed, based on the primary structure of the extracellular tight junction protein occludin. Peptides corresponding to the N-terminus of the first extracellular loop increased the permeability of the tight junctions, but lacked apical effect. This problem was solved by conjugation of one peptide to a lipoamino acid, resulting in two diastereomers with different effects. The L-isomer had a sustained apical effect, while that of the D-isomer was transient. In conclusion, conjugated occludin peptides constitute a new class of tight junction modulators that can enhance the tight junction permeability.
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Grenade, Danielle Sarah-Jane. "The role of the Hâº-electrochemical gradient in epithelial amino acid transport." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.421190.
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Nicholson, Benjamin. "The regulation of high affinity glutamate transport a bovine renal epithelial cell line." Thesis, University of Bristol, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336919.
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Darweesh, Ruba. "IN VITRO LUNG EPITHELIAL CELL TRANSPORT AND ANTI-INFLAMMATORY ACTIVITY FOR LIPOSOMAL CIPROFLOXACIN." VCU Scholars Compass, 2013. http://scholarscompass.vcu.edu/etd/577.
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Liposomal ciprofloxacin (Lipo-CPFX) is being developed for inhalation, with a goal of sustaining the therapeutic activity, compared to unformulated ciprofloxacin (CPFX). However, the kinetics and mechanism of its sustained local lung retention and pharmacological activity are yet to be fully characterized. This project hypothesized that Lipo-CPFX enables slower and sustained lung epithelial transport and uptake, compared to CPFX, thereby producing prolonged local pharmacological actions. The human bronchial epithelial Calu-3 cells were used as monolayers to characterize the kinetics and mechanism of transport and/or uptake, and to assess the effects of such slow kinetics for Lipo-CPFX on its inhibition against lipopolysaccharide (LPS)-induced proinflammatory IL-8 release. The transport fluxes for Lipo-CPFX across the highly restricted Calu-3 cell monolayers was transepithelial electrical resistance-independent, which suggested predominant transcellular transport. Compared to CPFX, Lipo-CPFX showed 6-18 times slower transport, while the flux was increased with increasing concentration proportionally without saturation. Its unaltered transport by cellular energy depletion, transport inhibition by a reduced temperature (4 oC) and endocytosis/lipid fusion inhibitors, filipin and LysoPC, and increased transport by excess empty liposomes collectively suggested cell energy-independent, lipid bilayer fusion mechanisms for the Lipo-CPFX transport across the Calu-3 cells. Likewise, Lipo-CPFX showed 2-4 fold lower cellular uptake than CPFX, proportional to concentration. Lipo-CPFX exhibited significant inhibitory activities at ≥ 0.01 mg/mL on LPS-induced IL-8 release from the Calu-3 cells, which was equipotent to CPFX. Upon 24 h pre-incubation, Lipo-CPFX caused 36.9 and 47.5 % inhibition at 0.01 and 0.05 mg/mL, respectively, while CPFX failed to do so. However, the effect was negated upon repeated wash of the mucosal cell surface, speculating the importance of cell membrane-associated drug/formulation on the inhibitory activities for Lipo-CPFX. Upon 24 h transport, Lipo-CPFX retained 79.0 % of the 4 µg dose on the mucosal cell surface, which was 1.9-times greater than 40.7 % for CPFX. As a result, when LPS was added at 24 h of the transport, Lipo-CPFX was still capable of causing 60.1 % inhibition, as its sustained local anti-inflammatory activity; CPFX however also exhibited equipotent inhibition, by virtue of comparable cellular drug uptake/transport.
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Villani, Natalie. "Use of a novel epithelial assay to screen for polyamine transport in Drosophila melanogaster." Honors in the Major Thesis, University of Central Florida, 2007. http://digital.library.ucf.edu/cdm/ref/collection/ETH/id/1049.
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This item is only available in print in the UCF Libraries. If this is your Honors Thesis, you can help us make it available online for use by researchers around the world by following the instructions on the distribution consent form at http://library.ucf.edu/Systems/DigitalInitiatives/DigitalCollections/InternetDistributionConsentAgreementForm.pdf You may also contact the project coordinator, Kerri Bottorff, at kerri.bottorff@ucf.edu for more information.Bachelors
Burnett College of Biomedical Sciences
Molecular Biology and Microbiology
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Planès, Carole. "Effet de l'hypoxie sur les proprietes de transport du sodium des cellules epitheliales alveolaires en culture." Paris 7, 1996. http://www.theses.fr/1996PA077263.
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Les effets de l'hypoxie sur les proprietes de transport du sodium (na) des cellules epitheliales alveolaires en culture ont ete etudies: (i) dans un modele d'hypoxie dans les cellules de la lignee sv40-t2 (obtenues par transfection de pneumocytes ii de rat neonatals par le gene de l'antigene t du virus sv40), dont nous avons verifie qu'elles possedaient la plupart des caracteristiques de transport du na des pneumocytes ii (pii) de rat en culture, (ii) dans un modele d'hypoxie-reoxygenation dans des pii de rat en culture primaire. L'exposition a l'hypoxie des cellules sv40-t2 induit une inhibition de l'activite de la na,k-atpase. Cette inhibition peut etre expliquee par une perturbation de l'homeostasie calcique secondaire a une augmentation de l'influx de calcium extracellulaire, puisqu'elle est completement prevenue par la nifedipine. L'augmentation de l'influx de calcium extracellulaire est en partie due a la liberation par les cellules sv40-t2 hypoxiques d'un facteur lipidique non identifie dans le milieu extracellulaire. Dans les pii de rat en culture, l'hypoxie induit de facon concomitante: (i) une inhibition de l'activite des canaux sodiques sensibles a l'amiloride, qui est parallele a la diminution d'expression des arnm des trois sous-unites du canal sodique epithelial de rat (renac), (ii) une diminution de l'activite de la na,k-atpase et de l'expression des arnm des sous-unites #1 et #1 de cette enzyme. L'expression et l'activite des canaux sodiques et de la na,k-atpase se normalisent en 48 heures de reoxygenation
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Helwig, Maren [Verfasser], Richard [Gutachter] Lucius, Georg [Gutachter] Pauli, and Lutz [Gutachter] Gürtler. "Transport von HIV-1 durch epitheliale Zellen / Maren Helwig ; Gutachter: Richard Lucius, Georg Pauli, Lutz Gürtler." Berlin : Humboldt-Universität zu Berlin, 2007. http://d-nb.info/120808058X/34.
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Tröger, Hanno [Verfasser]. "Wirkungsweise von Pathogenen, Pathobionten und Probiotika auf die epitheliale Transport- und Barrierefunktion des Darms / Hanno Tröger." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2017. http://d-nb.info/1123071632/34.
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Kim, Kyunghee. "Inward-rectifier chloride currents in Reissner’s membrane epithelial cells." Thesis, Kansas State University, 2010. http://hdl.handle.net/2097/3866.
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Master of ScienceDepartment of Anatomy and Physiology
Daniel C. Marcus
Sensory transduction in the cochlea depends on regulated ion secretion and absorption. Results of whole-organ experiments suggested that Reissner’s membrane may play a role in the control of luminal Cl-. We tested for the presence of Cl- transport pathways in isolated mouse Reissner’s membrane using whole-cell patch clamp recordings and gene transcript analyses using RT-PCR. The current-voltage (I-V) relationship in the presence of symmetrical NMDG-Cl was strongly inward-rectifying at negative voltages, with a small outward current at positive voltages. The inward-rectifying component of the I-V curve had several properties similar to those of the ClC-2 Cl- channel. It was stimulated by extracellular acidity and inhibited by extracellular Cd2+, Zn2+, and intracellular ClC-2 antibody. Channel transcripts expressed in Reissner’s membrane include ClC-2, Slc26a7 and ClC-Ka, but not Cftr, ClC-1, ClCa1, ClCa2, ClCa3, ClCa4, Slc26a9, ClC-Kb, Best1, Best2, Best3 or the beta-subunit of ClC-K, barttin. ClC-2 is the only molecularly-identified channel present that is a strong inward rectifier. This thesis incorporates the publication by K.X. Kim and D.C. Marcus, Inward-rectifier chloride currents in Reissner’s membrane epithelial cells. Biochem. Biophys. Res. Commun. 394 (2010) 434-438, with permission of the publisher Elsevier, and is the first report of conductive Cl- transport in epithelial cells of Reissner’s membrane and is consistent with an important role in endolymph anion homeostasis.
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Yau, Kwok-hei, and 邱國禧. "Small molecule-based synthetic ion channels modulate smooth muscle contraction and epithelial ion transport." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hdl.handle.net/10722/196079.
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In living systems, ion channels are membrane transport proteins that provide pathways for the passive diffusion of ions through lipid membranes. The flow of ions across membranes is the basis of many important physiological processes, including but not limited to the regulation of membrane potential, transepithelial transport and cell volume. While many efforts have been made to understand the biological roles of natural ion channels, the biological activities of artificial ion channels remain largely unknown. Recently, it was reported that a small molecule 1, which forms synthetic chloride (Cl–) channels in membranes via self-assembly, is capable of modulating vascular functions. In this thesis, novel small molecules that are structurally similar to 1 are shown to form artificial ion channels in membranes. Together with 1, the effects of these small molecules on the contractile activities of smooth muscles and epithelial ion transport are explored. The therapeutic implications of the findings are also discussed.
A collection of small molecules was screened using liposome-based fluorescence assays. In these assays, the ability of the synthetic compounds to modulate membrane potential was monitored. The screening yielded compound 3 that formed synthetic potassium (K+) channels in liposomal membranes, although the liposome-based fluorescence experiments suggested that 3 also transported Cl–. Two derivatives of 3, namely, compounds 2 and 4 were also examined. Single-channel recording experiments suggested that 2 forms synthetic Cl– channels in liposomal membranes.
The effects of compounds 2 and 3 on the functions of the vascular smooth muscle are explored. Using confocal imaging, it was shown that both 2 and 3 counteracted the effects of high-K+ depolarizing solution on membrane potential and intracellular Ca2+ concentration ([Ca2+]i) in cultured vascular smooth muscle cells. 2 and 3 also relaxed mice aortic rings pre-contracted with high-K+ solution. These observations can be explained in terms of the Cl– transporting functions of 2 and 3.
To determine the potential for developing the compounds into bronchodilators, the effects of compounds 1 and 3 on the contractile activities of the airway smooth muscle (ASM) were explored using organ bath technique. The contractile activities of the trachea isolated from Sprague-Dawley (SD) rats were first characterized. Among the contractile agents used, only potassium chloride (KCl), cholinergic agonists, serotonin and endothelin-1 were contractile to the SD rat trachea. 1 and 3 relaxed the ASM pre-contracted with KCl, whereas the contractions induced by other agonists were not affected.
The ability of compounds 2, 3 and 4 to modulate ion transport across cultured epithelia was tested by the short-circuit current measurement technique. It was shown that the compounds were capable of inducing Cl– secretion when applied to the apical side of airway and colonic epithelia. Importantly, the synthetic compounds induced apical Cl– secretion in immortalized cystic fibrosis (CF) bronchial epithelia. This suggests that the synthetic compounds may be used to correct the anion transport defect in CF epithelia.
In summary, the small-molecule based synthetic ion channels demonstrated two important general functions of natural ion channels, namely, the regulation of membrane potential and epithelial ion transport.published_or_final_version
Chemistry
Doctoral
Doctor of Philosophy
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Beck, Laurent. "Incorporation, transport et role du sulfate dans les cellules epitheliales glandulaires de l'endometre de cobaye en culture : etude de l'action de la progesterone." Besançon, 1992. http://www.theses.fr/1992BESA3719.
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ZAAFRANI, MINA. "Etude des reponses electriques associees au transport des acides amines neutres dans la cellule epitheliale embryonnaire d'amphibien." Paris 11, 1991. http://www.theses.fr/1991PA112161.
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Nous avons montre, dans une etude electrophysiologique, que l'exposition d'enterocytes embryonnaires de xenope a differents acides amines neutres (aan) tels que gly, l-ala, l-ser, l-pro, l-asn et l-gln, l-leu, l-phe induit un courant transmembranaire attribuable a un co-transport d'ions et d'aan. Les reponses electriques aux six premiers aan sont na- et voltage-dependantes. Paradoxalement, les reponses a l-leu et l-phe (aa connus pour ne pas etre co-transportes avec na) induisent un courant entrant, concentration en aa-dependant comme les premiers, mais ce courant s'est avere insensible aux variations de na#e et k#e, il ne peut etre explique par les variations de cl#e et co#3h#e, il est insensible aux variations du potentiel de membrane. Nous avons compare la sensibilite des reponses electriques aux deux groupes d'aa a differents agents inhibiteurs du transport tels que meaib, bch, amiloride, ouabaine, la reduction de na externe, l'augmentation de k externe, et la depolarisation membranaire. Nous avons cherche a identifier leurs sites d'action et observe que la reponse a l-leu et l-phe est insensible a ces inhibiteurs hormis bch. Cette etude a revele que la reponse aux autres aa ne peut etre totalement abolie. En outre, la fraction de courant qui subsiste est en presence d'inhibiteurs presente des proprietes similaires a celles des reponses induites par l-leu ou l-phe. Elle varie selon une fonction saturable de la concentration en aan; elle est insensible aux variations du potentiel de membrane comme aux alterations de la composition ionique du milieu extracellulaire a l'exception du ph. La sensibilite aux variations de ph#e, l'effet potentiateur du co#3h# constate et l'inhibition marquee de ces reponses electriques par le 2,4-dnp nous ont amenee a postuler que cette composante de courant pourrait etre, comme la reponse a l-leu et l-phe, portee par un influx de protons accompagnant l'im
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Vermaak, I., AM Viljoen, JH Hamman, and Vuuren SF Van. "Effect of simulated gastrointestinal conditions and epithelial transport on extracts of green tea and sage." Elsevier, 2009. http://encore.tut.ac.za/iii/cpro/DigitalItemViewPage.external?sp=1001730.
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A bstract
Few in vitro screening studies on the biological activities of plant extracts that are intended for oral
administration consider the effect of the gastrointestinal system. This study investigated this aspect on
extracts of Camellia sinensis (green tea) and Salvia officinalis (sage) using antimicrobial activity as amodel
for demonstration. Both the crude extracts and their products after exposure to simulated gastric fluid
(SGF) as well as simulated intestinal fluid (SIF) were screened for antimicrobial activity. The
chromatographic profiles of the crude plant extracts and their SGF as well as SIF products were recorded
and compared qualitatively by means of high performance liquid chromatography coupled to mass
spectrometry. The effect of epithelial transport on the crude plant extracts was determined by applying
them to an in vitro intestinal epithelial model (Caco-2). The crude extracts for both plants exhibited
reduced antimicrobial activity after exposure to SGF, while no antimicrobial activity was detected after
exposure to SIF. These results suggested chemical modification or degradation of the antimicrobial
compounds when exposed to gastrointestinal conditions. This was confirmed by a reduction of the peak
areas on the LC–UV–MS chromatograms. From the chromatographic profiles obtained during the
transport study, it is evident that some compounds in the crude plant extracts were either not
transported across the cell monolayer or they were metabolised during passage through the cells. It can
be deduced that the gastrointestinal environment and epithelial transport process can dramatically
affect the chromatographic profiles and biological activity of orally ingested natural products.
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Scott, Derek A. "Characterisation and regulation of iron- and zinc-evoked electrogenic transport in human intestinal epithelial cells." Thesis, University of Aberdeen, 2004. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU193466.
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Application of iron or zinc to the apical surface of Caco-2 cells induced an inward short-circuit current (Isc). These I sc responses were concentration-, pH- and temperature-dependent in nature. Fe2+ and Zn2+-induced transport was electrogenic and resulted in intracellular acidification. Transepithelial proton-coupled transport appeared to involve distinct transport mechanisms for each metal. The apical charge needed to generate the Isc responses was carried by the metal ion and protons, whereas basolateral charge carriage was accomplished by protons alone. Transport may occur in any isotonic media, provided that an inwardly-directed proton gradient is supplied across the apical membrane. The magnitude of the Isc responses evoked by Fe2+ and Zn 2+ was dependent upon the development of Caco-2 cells. When DMT1 (IRE) mRNA levels from cells were analysed by real-time PCR, they appeared to follow a similar pattern. These transport processes may be regulated physiologically at the level of the intestine since enterocyte metal status may induce changes in the expression of DMT1 isoforms. Fe2+ and Zn2+ appeared to have different effects on transporter expression and the Isc responses evoked. Pathophysiological and potential physiological regulation of Fe2+ and Zn2+-evoked transport was demonstrated by using 8Br-cGMP to mimic the elevation of intracellular cGMP levels observed during secretory diarrhoea. Exposure of Caco-2 epithelia to 8Br-cGMP inhibited Fe2+ and Zn2+-evoked transport. By using protein kinase inhibitors, it appeared that 8Br-cGMP-depdnent inhibition of transport was mediated by PKG II. Identification of this pathway provides support for its manipulation as a potential strategy in preventing the diarrhoeal-induced iron and zinc malabsorption associated with enterotoxic diarrhoeal diseases.
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Rytkönen, J. (Jani). "Effect of heat denaturation of bovine milk beta-lactoglobulin on its epithelial transport and allergenicity." Doctoral thesis, University of Oulu, 2006. http://urn.fi/urn:isbn:9514281209.
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Abstract
Beta-lactoglobulin (β-lg) is the main whey protein in bovine milk. It belongs to the lipocalin protein family, and it is one of the main milk allergens. Resistance to hydrolysis is a particular feature of β-lg making it possible that β-lg reaches the small intestine in its native form. Heat treatments during milk processing may change the native structure of bovine β-lg and change its intestinal transport properties. Heat induced conformational alterations may also expose new antigenic sites. However, there have been no previous studies on the effects of heat treatment on the transport of β-lg or on its sensitizing properties.
Cow's milk allergy is one of the most important food allergies affecting about 2.4% of infants. Milk proteins, including β-lg, in breast milk substitute formulas are often the earliest foreign antigens in the diet of newborns. According to the hygiene hypothesis, natural infections and vaccinations may modify the immunological balance and decrease the risk of allergy.
Isoelectric precipitations followed by anion exchange and gel filtration were used to purify bovine milk β-lg in its native form. Transport of native and heat-denatured β-lg was compared in two in vitro cell models, Caco-2 and M-cells. Sensitization properties of native and heat-denatured β-lg were studied with an animal model using Hooded-Lister rats. Effects of BCG vaccination in combination with the native β-lg were also studied. Effects of different sensitizations were assessed by antibody levels in serum and inflammation locally in the gastrointestinal tract.
Heat denaturation of β-lg made its transport slower in both enterocytes and M-cells. M-cells were more effective transporters of both native and heat-denatured β-lg than caco-2 cells. Animals generated higher levels of IgE when sensitized with native β-lg, but heat-denatured β-lg induced a more intense inflammatory cell reaction in the gastrointestinal tract. Vaccination with BCG decreased serum IgE concentration and modified the predominant site of the inflammatory cell response in intestine.
The results indicate that, heat denaturation of β-lg and BCG vaccination, change both the systemic and the mucosal response to bovine milk β-lg. The reasons for this remain speculative. The effect of BCG vaccination is consistent with the hygiene hypothesis. The observed alteration of transport properties could be one mechanism by which heat denaturation modifies the allergenic properties of this protein, but additional studies are necessary to assess whether other mechanisms, such as exposure of new antigenic determinants are also relevant.
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Mansley, Morag K. "The signalling pathways allowing hormonal regulation of Na+ transport in murine collecting duct cells." Thesis, University of Dundee, 2010. https://discovery.dundee.ac.uk/en/studentTheses/620faf6a-2ed6-4cad-b239-227f2827101d.
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The collecting duct of the distal nephron marks the final location where adjustments to Na+ excretion can be made, therefore determining the final concentration of Na+ conserved in the extracellular fluid which plays a role in governing overall blood volume and pressure. This transport of Na+ is subject to hormonal regulation but the signalling pathways underpinning this regulation however, are not fully understood. In this thesis the signalling pathways allowing both basal and insulin-stimulated Na+ absorption were explored in the murine collecting duct cell line, mpkCCDcl4. The effects of two insulin-sensitizing drugs, TZDs, on ENaC-mediated Na+ transport were investigated and the signalling pathways underlying two other hormonal regulators of ENaC, dexamethasone and vasopressin, were also examined. Unstimulated monolayers of mpkCCDcl4 cells generated spontaneous Na+ absorption which was quantified by measuring equivalent short circuit current (Ieq). Selective inhibition of PI3-kinase, mTORC2 and SGK1 left ~80 % of the current intact, indicating these signalling molecules are not required for basal Na+ transport. Acute addition of insulin stimulated Ieq and this occurred with a concomitant increase in mTORC2, SGK1 and Akt activity. Inhibition of PI3-kinase abolished the insulin-stimulated response as well as phosphorylation of downstream substrates, indicating a crucial role of PI3-kinase. Inhibition of mTORC1 with rapamycin did not alter basal or insulin-stimulated Na+ transport. The mTOR inhibitors TORIN1 and PP242 could therefore be used to evaluate the role of mTORC2. These inhibitors greatly reduced insulin-stimulated ENaC-mediated Na+ transport and also abolished SGK1 and mTORC2 activity, indicating a novel role of mTORC2. An inhibitor of SGK1, GSK650394A abolished insulin-stimulated Na+ transport and specifically inhibited SGK1 acitivty demonstrating the importance of SGK1 in insulin signalling. The inhibitor Akti-1/2 also abolished insulin-mediated Na+ transport but this compound inhibited both Akt and SGK1 activity. The TZDs pioglitazone and rosiglitazone did not alter basal or insulin-stimulated Na+ transport and had no effect on SGK1 activity indicating these drugs do not alter Na+ absorption in this cell line. Dexamethasone stimulated ENaC-mediated Na+ transport in a similar manner to insulin and this could be blocked with rapamycin. This drug did not alter phosphorylation of NDRG1 indicating that dexamethasone stimulates Na+ transport in an mTORC1-dependent manner but without altering SGK1 activity. Arginine vasopressin also stimulated Ieq but did so by reducing Rt with an associated depolarisation of Vt. Ieq could be blocked with amiloride and vasopressin-stimulated Ieq was insensitive to TORIN1 and PP242. Vasopressin suppressed SGK1 phosphorylation of NDRG1 but did stimulate protein kinase A (PKA) activity. Therefore vasopressin stimulates Ieq via a PKA-dependent but mTOR- and SGK1-independent pathway.
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VAN, DER GOOT FRANCOISE. "Role respectif des membranes apicales et basolaterales dans les mecanismes de transport d'eau a travers les structures epitheliales." Paris 6, 1990. http://www.theses.fr/1990PA066706.
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Le role respectif des membranes apicales et basolaterales de cellules epitheliales dans le transport de l'eau a ete etudie sur deux tissus de nature tres differente: 1) le tubule proximal de rein de lapin, qui sous l'influence d'un gradient osmotique de faible amplitude transporte des quantites d'eau tres importantes; 2) la vessie de grenouille, utilisee comme modele du canal collecteur renal, qui est generalement soumise a un tres important gradient osmotique et dont la permeabilite est controlee par l'hormone antidiuretique (adh). Par des mesures de spectrophotometrie a flux interrompu, nous avons pu montrer que les permeabilites osmotiques (pf) des membranes apicales et basolaterales du tubule proximal sont tres elevees. L'inhibition de pf par des agents sulfhydryls, suggere la presence, dans ces deux membranes plasmiques, de canaux proteiques responsables du passage de l'eau. L'obtention de coefficients de reflexion de nacl et de kcl proches de 1 indiquent une certaine selectivite de cas canaux vis-a-vis de l'eau. Concernant la vessie de grenouille, des mesures de diffusion d'eau tritiee a travers des vessies dont la membrane apicale avait ete traitee par l'amphotericine b, ont montre que la permeabilite diffusionnelle a l'eau (pd) de la membrane basolaterale etait tres elevee, independamment de toute stimulation par l'adh. La sensibilite de pd a certains agents sulfhydryls met en evidence l'existence de canaux proteiques transmembranaires apparemment semblables a deux rencontres dans les membranes cellulaires du tubule proximal. Finalement, nous proposons une approche originale visant a isoler les canaux hydriques qui apparaissent dans la membrane apicale de la vessie de grenouille, lors d'une stimulation par l'adh. Les vesicules d'endocytose, qui apparaissent dans les cellules a granules de la vessie apres retrait de l'hormone, ont ete marquees a l'aide d'un marqueur fluorescent puis triees par cytometrie en flux. L'electrophorese sur gel de polyacrylamide de ces endosomes fait apparaitre deux bandes majoritaires de 55 et 67 kda. Ces deux proteines pourraient faire partie, ou etre, les canaux hydriques mis en evidence lors des precedentes mesures de permeabilite
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Cormet-Boyaka, Estelle. "Le transport des fluoroquinolones dans la cellule epitheliale intestinale ; les mecanismes d'absorption et de secretion de la sparfloxacine." Paris 11, 1997. http://www.theses.fr/1997PA114855.
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Friedlander, Gérard. "Etude des facteurs qui modulent l'effet des hormones sur des cellules epitheliales d'origine renale." Paris 7, 1987. http://www.theses.fr/1987PA077204.
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Wang, Qian. "Regulation of sodium transport across epithelia derived from human mammary gland." Diss., Kansas State University, 2014. http://hdl.handle.net/2097/17600.
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Doctor of PhilosophyDepartment of Anatomy and Physiology
Bruce D. Schultz
The first aim of this project is to define the cellular mechanisms that account for the low Na[superscript]+ concentration in human milk. MCF10A cells, which were derived from human mammary epithelium and grown on permeable supports, exhibit amiloride- and benzamil-sensitive short circuit current (I[subscript]sc), suggesting activity of the epithelial Na[superscript]+ channel, ENaC. When cultured in the presence of cholera toxin (Ctx), MCF10A cells exhibit greater amiloride sensitive I[subscript]sc at all time points tested, an effect that is not reduced with Ctx washout for 12 hours or by cytosolic pathways inhibitors. Ctx increases the abundance of both beta and gamma-ENaC in the apical membrane and increases its monoubiquitination but without changing total protein and mRNA levels. Additionally, Ctx increases the levels of both the phosphorylated and the nonphosphorylated forms of Nedd4-2, a ubiquitin-protein ligase that regulates ENaC degradation. The results reveal a novel mechanism in human mammary gland epithelia by which Ctx regulates ENaC-mediated Na[superscript]+ transport. The second project aim is to develop a protocol to isolate mammary gland epithelia for subsequent in vitro culture. Caprine (1[superscript]0CME) and bovine mammary epithelia (1[superscript]0BME) were isolated and cultured on permeable supports to study hormone- and neurotransmitter-sensitive ion transport. Both 1[superscript]0CME and 1[superscript]0BME cells were passed for multiple subcultures and all passages formed electrically tight barriers. 1[superscript]0CME were cultured in the presence of hydrocortisone and exhibited high electrical resistance and amiloride-sensitive I[subscript]sc, suggesting the presence of ENaC-mediated Na[superscript]+ transport. 1[superscript]0BME were grown in a complex media in the presence or absence of dexamethasone. In contrast to 1[superscript]0CME, 1[superscript]0BME exhibited no detectable amiloride-sensitive I[subscript]sc in either culture condition. However, 1[superscript]0BME monolayers responded to an adrenergic agonist, norepinephrine, and a cholinergic agonist, carbamylcholine, with rapid increases in I[subscript]sc. Thus, this protocol for isolation and primary cell culture can be used for future studies that focus on mammary epithelial cell regulation and functions. In conclusion, the results from these projects demonstrate that mammary epithelial cells form electrically tight monolayers and can exhibit neurotransmitter- and/or hormone-induced net ion transport. The mechanisms that regulate Na[superscript]+ transport across mammary gland may provide clues to prevent or treat mastitis.
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Thomson, Susmita. "Local feedback regulation of salt & water transport across pumping epithelia : experimental & mathematical investigations in the isolated abdominal skin of Bufo marinus /." Connect to this title, 2002. http://theses.library.uwa.edu.au/adt-WU2003.0022.
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