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Yoshiko Nakae - One of the best experts on this subject based on the ideXlab platform.

Hiroshi Ishiguro - One of the best experts on this subject based on the ideXlab platform.

  • caffeine inhibits fluid secretion by Interlobular Ducts from guinea pig pancreas
    Pancreas, 2017
    Co-Authors: Yuka Mochimaru, Akiko Yamamoto, Miyuki Nakakuki, Makoto Yamaguchi, Ituka Taniguchi, Hiroshi Ishiguro
    Abstract:

    ObjectivesCaffeine is contained in coffee, tea, and numerous beverages and foods. We examined the direct effects of caffeine on the physiological function of pancreatic Duct cells by using Interlobular Duct segments isolated from guinea pig pancreas.MethodsThe rate of fluid secretion was continuousl

  • MECHANISMS OF HCO3- SECRETION BY PANCREATIC Duct
    2015
    Co-Authors: Makoto Yamaguchi, Hiroshi Ishiguro, Akiko Yamamoto, Yoshiro Sohma, Martin Steward, Akito Shimouchi, Takaharu Kondo
    Abstract:

    Pancreatic Duct epithelium secretes a HCO3--rich isotonic fluid that is dependent on the activity of the cystic fibrosis transmembrane conDuctance regula-tor (CFTR) at the apical membrane. The HCO3- con-centration of human and guinea-pig pancreatic juice reaches140 mM at maximal stimulation with se-cretin. Fig. 1 shows the current model for HCO3-transport by pancreatic Duct cells. Accumulation of HCO3- across the basolateral membrane is mediated by Na+-HCO3- cotransport and Na+-H+ exchange. In guinea-pig pancreatic Duct, Na+-HCO3- cotransport accounts for75 % of HCO3- accumulation. HCO3- se-cretion across the apical membrane is mediated (i) by Cl-/HCO3- exchange via an SLC26A6 anion trans-porter and (ii) by the HCO3- conDuctance of CFTR. The relative contribution of these two apical mecha-nisms varies depending on the anion composition of the luminal fluid (1). This model is based on measurements of intracellular pH (pHi), Cl- concen-tration ([Cl-]i), and membrane potential (Pd) in lumi-nally-microperfused Interlobular Duct segments iso-lated from guinea-pig pancreas (2). MINI-REVIEW Apical Cl-/HCO3- exchanger stoichiometry in the modeling of HCO3- transport by pancreatic Duct epitheliu

  • membrane potential and bicarbonate secretion in isolated Interlobular Ducts from guinea pig pancreas
    The Journal of General Physiology, 2002
    Co-Authors: Hiroshi Ishiguro, Martin C Steward, Motoji Kitagawa, T Hayakawa, R M Case, Yoshiro Sohma, T Kubota, Takaharu Kondo, Satoru Naruse
    Abstract:

    The Interlobular Duct cells of the guinea-pig pancreas secrete HCO3− across their luminal membrane into a HCO3−-rich (125 mM) luminal fluid against a sixfold concentration gradient. Since HCO3− transport cannot be achieved by luminal Cl−/HCO3− exchange under these conditions, we have investigated the possibility that it is mediated by an anion conDuctance. To determine whether the electrochemical potential gradient across the luminal membrane would favor HCO3− efflux, we have measured the intracellular potential (Vm) in microperfused, Interlobular Duct segments under various physiological conditions. When the lumen was perfused with a 124 mM Cl−-25 mM HCO3− solution, a condition similar to the basal state, the resting potential was approximately −60 mV. Stimulation with dbcAMP or secretin caused a transient hyperpolarization (∼5 mV) due to activation of electrogenic Na+-HCO3− cotransport at the basolateral membrane. This was followed by depolarization to a steady-state value of approximately −50 mV as a result of anion efflux across the luminal membrane. Raising the luminal HCO3− concentration to 125 mM caused a hyperpolarization (∼10 mV) in both stimulated and unstimulated Ducts. These results can be explained by a model in which the depolarizing effect of Cl− efflux across the luminal membrane is minimized by the depletion of intracellular Cl− and offset by the hyperpolarizing effects of Na+-HCO3− cotransport at the basolateral membrane. The net effect is a luminally directed electrochemical potential gradient for HCO3− that is sustained during maximal stimulation. Our calculations indicate that the electrodiffusive efflux of HCO3− to the lumen via CFTR, driven by this gradient, would be sufficient to fully account for the observed secretory flux of HCO3−.

  • fluid secretion in Interlobular Ducts isolated from guinea pig pancreas
    The Journal of Physiology, 1998
    Co-Authors: Hiroshi Ishiguro, Satoru Naruse, Martin C Steward, Motoji Kitagawa, T Hayakawa, R M Case
    Abstract:

    1 Pancreatic HCO3− and fluid secretion were studied by monitoring luminal pH (pHL) and luminal volume simultaneously in Interlobular Duct segments isolated from guinea-pig pancreas. The secretory rate and HCO3− flux were estimated from fluorescence images obtained following microinjection of BCECF-dextran (70 kDa, 20 μM) into the Duct lumen. 2 Ducts filled initially with a Cl−-rich solution swelled steadily (2.0 nl min−1 mm−2) when HCO3−/CO2 was introduced, and the luminal pH increased to 8.08. When Cl− was replaced by glucuronate, spontaneous fluid secretion was reduced by 75 %, and pHL did not rise above 7.3. 3 Cl−-dependent spontaneous secretion was largely blocked by luminal H2DIDS (500 μM). We conclude that, in unstimulated Ducts, HCO3− transport across the luminal membrane is probably mediated by Cl−-HCO3− exchange. 4 Secretin (10 nM) and forskolin (1 μM) both stimulated HCO3− and fluid secretion. The final value of pHL (8.4) and the increase in secretory rate (1.5 nl min−1 mm−2) after secretin stimulation were unaffected by substitution of Cl−. 5 The Cl−-independent component of secretin-evoked secretion was not affected by luminal H2DIDS. This suggests that a Cl−-independent mechanism provides the main pathway for luminal HCO3− transport in secretin-stimulated Ducts. 6 Ducts filled initially with a HCO3−-rich fluid (125 mM HCO3−, 23 mM Cl−) secreted a Cl−-rich fluid while unstimulated. This became HCO3−-rich when secretin was applied. 7 Addition of H2DIDS and MIA (10 μM) to the bath reduced the secretory rate by 56 and 18 %, respectively. Applied together they completely blocked fluid secretion. We conclude that basolateral HCO3− transport is mediated mainly by Na+-HCO3− cotransport rather than by Na+-H+ exchange.

Yasuko Ishikawa - One of the best experts on this subject based on the ideXlab platform.

Noriko Inoue - One of the best experts on this subject based on the ideXlab platform.

Marsha L. Frazier - One of the best experts on this subject based on the ideXlab platform.

  • mouse pancreatic acinar Ductular tissue gives rise to epithelial cultures that are morphologically biochemically and functionally indistinguishable from Interlobular Duct cell cultures
    In Vitro Cellular & Developmental Biology – Animal, 1994
    Co-Authors: Sherwood Githens, Jane A. Schexnayder, Randy L. Moses, Gerene M. Denning, Jeffrey J. Smith, Marsha L. Frazier
    Abstract:

    Most of the pancreatic exocrine epithelium consists of acinar and intralobular Duct (Ductular) cells, with the balance consisting of Interlobular and main Duct cells. Fragments of mouse acinar/Ductular epithelium can be isolated by partial digestion with collagenase and purified by Ficoll density gradient centrifugation. We investigated whether previously developed culture conditions used for Duct epithelium would result in the selective survival and proliferation of Ductular cells from the acinar/Ductular fragments. The fragments were cultured on nitrocellulose filters coated with extracellular matrix. After 2 to 4 wk the filters were covered with proliferating cells resembling parallel cultures of Duct epithelium by the following criteria: protein/DNA ratio, light and electron microscopic appearance, the presence of Duct markers (carbonic anhydrase [CA] activity, CA II mRNA, the cystic fibrosis transmembrane conDuctance regulator), the near absence of acinar cell markers (amylase and chymotrypsin), a similar polypeptide profile after sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the presence of spontaneous and secretin-stimulated electrogenic ion transport. Both Duct and Ductular epithelia formed fluid-filled cysts in collagen gels and both could be subcultured. We conclude that acinar/Ductular tissue gives rise to Ductular cells in culture by some combination of acinar cell death and/or transdifferentiation to a Ductular phenotype, accompanied by proliferation of these cells and preexisting Ductular cells. These cultures may be used to investigate the properties of this part of the pancreatic Duct system, from which most of the pancreatic juice water and electrolytes probably originates.

  • Mouse pancreatic acinar/Ductular tissue gives rise to epithelial cultures that are morphologically, biochemically, and functionally indistinguishable from Interlobular Duct cell cultures.
    In Vitro Cellular & Developmental Biology - Animal, 1994
    Co-Authors: Sherwood Githens, Jane A. Schexnayder, Randy L. Moses, Gerene M. Denning, Jeffrey J. Smith, Marsha L. Frazier
    Abstract:

    Most of the pancreatic exocrine epithelium consists of acinar and intralobular Duct (Ductular) cells, with the balance consisting of Interlobular and main Duct cells. Fragments of mouse acinar/Ductular epithelium can be isolated by partial digestion with collagenase and purified by Ficoll density gradient centrifugation. We investigated whether previously developed culture conditions used for Duct epithelium would result in the selective survival and proliferation of Ductular cells from the acinar/Ductular fragments. The fragments were cultured on nitrocellulose filters coated with extracellular matrix. After 2 to 4 wk the filters were covered with proliferating cells resembling parallel cultures of Duct epithelium by the following criteria: protein/DNA ratio, light and electron microscopic appearance, the presence of Duct markers (carbonic anhydrase [CA] activity, CA II mRNA, the cystic fibrosis transmembrane conDuctance regulator), the near absence of acinar cell markers (amylase and chymotrypsin), a similar polypeptide profile after sodium dodecyl sulfate-polyacrylamide gel electrophoresis, and the presence of spontaneous and secretin-stimulated electrogenic ion transport. Both Duct and Ductular epithelia formed fluid-filled cysts in collagen gels and both could be subcultured. We conclude that acinar/Ductular tissue gives rise to Ductular cells in culture by some combination of acinar cell death and/or transdifferentiation to a Ductular phenotype, accompanied by proliferation of these cells and preexisting Ductular cells. These cultures may be used to investigate the properties of this part of the pancreatic Duct system, from which most of the pancreatic juice water and electrolytes probably originates.

  • Carbonic anhydrase II gene expression in mouse pancreatic Duct cells.
    Pancreas, 1992
    Co-Authors: Sherwood Githens, Jane A. Schexnayder, Marsha L. Frazier
    Abstract:

    Summary Our goal is to create a transgenic mouse model for human pancreatic Duct cell adenocarcinoma using the promoterlenhancer region of the carbonic anhydrase (CA) I1 gene to drive the expression of SV-40 T-antigen in pancreatic Duct cells. This requires that the CA I1 gene be expressed in mouse pancreatic Duct cells and not in other pancreatic cells, as has already been shown to be the case in the human and guinea pig pancreas. We have shown with an enzyme histochemical assay that mouse pancreatic Duct cells contain CA activity in both intact pancreas and cultured Interlobular Duct epithelium. In addition, CA activity was detected with a biochemical assay in homogenates of cultured Duct epithelium. The specific activity of Duct cells was 2.75–fold greater than in whole pancreas, suggesting that a substantial amount of total pancreatic CA activity is contributed by Duct cells. At least some of the CA in cultured Duct cells was inferred to be CA II by Northern blot analysis of RNA extracted from the cells. The concentration of CA 11 mRNA in the cultured Duct cells was substantially greater than in whole pancreas and would appear to account for the majority, if not all, of the CA I1 in the mouse pancreas.