scholarly journals Pattern of Ca2+increase determines the type of secretory mechanism activated in dog pancreatic duct epithelial cells

2006 ◽  
Vol 576 (1) ◽  
pp. 163-178 ◽  
Author(s):  
Seung-Ryoung Jung ◽  
Kyungjin Kim ◽  
Bertil Hille ◽  
Toan D. Nguyen ◽  
Duk-Su Koh
2014 ◽  
Vol 35 (8) ◽  
pp. 1840-1846 ◽  
Author(s):  
Yuki Inagawa ◽  
Kenji Yamada ◽  
Takashi Yugawa ◽  
Shin-ichi Ohno ◽  
Nobuyoshi Hiraoka ◽  
...  

Pancreas ◽  
1996 ◽  
Vol 12 (2) ◽  
pp. 109-116 ◽  
Author(s):  
Dolphine Oda ◽  
Christopher E. Savard ◽  
Lydia Eng ◽  
Sum P. Lee

PLoS ONE ◽  
2015 ◽  
Vol 10 (7) ◽  
pp. e0132978 ◽  
Author(s):  
Sarah Arfmann-Knübel ◽  
Birte Struck ◽  
Geeske Genrich ◽  
Ole Helm ◽  
Bence Sipos ◽  
...  

2000 ◽  
Vol 116 (4) ◽  
pp. 507-520 ◽  
Author(s):  
Duk-Su Koh ◽  
Mark W. Moody ◽  
Toan D. Nguyen ◽  
Bertil Hille

We asked if the mechanisms of exocytosis and its regulation in epithelial cells share features with those in excitable cells. Cultured dog pancreatic duct epithelial cells were loaded with an oxidizable neurotransmitter, dopamine or serotonin, and the subsequent release of these exogenous molecules during exocytosis was detected by carbon-fiber amperometry. Loaded cells displayed spontaneous exocytosis that may represent constitutive membrane transport. The quantal amperometric events induced by fusion of single vesicles had a rapid onset and decay, resembling those in adrenal chromaffin cells and serotonin-secreting leech neurons. Quantal events were frequently preceded by a “foot,” assumed to be leak of transmitters through a transient fusion pore, suggesting that those cell types share a common fusion mechanism. As in neurons and endocrine cells, exocytosis in the epithelial cells could be evoked by elevating cytoplasmic Ca2+ using ionomycin. Unlike in neurons, hyperosmotic solutions decreased exocytosis in the epithelial cells, and giant amperometric events composed of many concurrent quantal events were observed occasionally. Agents known to increase intracellular cAMP in the cells, such as forskolin, epinephrine, vasoactive intestinal peptide, or 8-Br-cAMP, increased the rate of exocytosis. The forskolin effect was inhibited by the Rp-isomer of cAMPS, a specific antagonist of protein kinase A, whereas the Sp-isomer, a specific agonist of PKA, evoked exocytosis. Thus, PKA is a downstream effector of cAMP. Finally, activation of protein kinase C by phorbol-12-myristate-13-acetate also increased exocytosis. The PMA effect was not mimicked by the inactive analogue, 4α-phorbol-12,13-didecanoate, and it was blocked by the PKC antagonist, bisindolylmaleimide I. Elevation of intracellular Ca2+ was not needed for the actions of forskolin or PMA. In summary, exocytosis in epithelial cells can be stimulated directly by Ca2+, PKA, or PKC, and is mediated by physical mechanisms similar to those in neurons and endocrine cells.


1997 ◽  
Vol 273 (1) ◽  
pp. G204-G216 ◽  
Author(s):  
L. al-Nakkash ◽  
C. U. Cotton

Secretion of salt and water by the epithelial cells that line pancreatic ducts depends on activation of apical membrane Cl- conductance. In the present study, we characterized two types of Cl- conductances present in the apical cell membrane of bovine pancreatic duct epithelial cells. Primary cultures of bovine main pancreatic duct epithelium and an immortalized cell line (BPD1) derived from primary cultures were used. Elevation of intracellular adenosine 3',5'-cyclic monophosphate (cAMP) or Ca2+ in intact monolayers of duct epithelium induced sustained anion secretion. Agonist-induced changes in plasma membrane Cl- permeability were accessed by 36 Cl- efflux, whole cell current recording, and measurements of transepithelial Cl- current across permeabilized epithelial monolayers. Elevation of intracellular cAMP elicited a sustained increase in Cl- permeability, whereas elevation of intracellular Ca2+ induced only a transient increase in Cl- permeability. Ca(2+)- but not cAMP-induced increases in Cl- permeability were abolished by preincubation of cells with the Ca2+ buffer 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, tetra(acetoxymethyl) ester (BAPTA-AM). N-phenylanthranilic acid (DPC; 1 mM) and glibenclamide (100 microM), but not 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS; 500 microM), inhibited the cAMP-induced increase in Cl- permeability. In contrast, DPC and DIDS, but not glibenclamide, inhibited the Ca(2+)-induced increase in Cl- permeability. We conclude from these experiments that bovine pancreatic duct epithelial cells express at least two types of Cl- channels, cAMP and Ca2+ activated, in the apical cell membrane. Because the Ca(2+)-activated increase in Cl- permeability is transient, the extent to which this pathway contributes to sustained anion secretion by the ductal epithelium remains to be determined.


1979 ◽  
Vol 150 (1) ◽  
pp. 1-9 ◽  
Author(s):  
E L Parr

Islets of Langerhans were isolated from mouse pancreases and fixed in periodatelysine-paraformaldehyde. The fixed islets were then dissociated with trypsin and EDTA to yield cell suspensions that contained mainly four cell types; beta-cells, capillary endothelial cells, acinar cells, and pancreatic duct epithelial cells. The nonislet cells were probably associated wtih the surface of the isolated islets. The H-2 antigens of the dissociated pancreatic cells were labeled with an immunoferritin technique. Pancreatic duct epithelial cells showed specific ferritin labeling on their lateral cell membranes but not on apical microvillus membranes. Acinar cells were also labeled on lateral membranes, and the capillary endothelial cells were labeled on both the luminal and albuminal aspects of their surface membranes. In contrast, pancreatic beta-cells were unlabeled. The number of ferritin molecules per unit length of beta-cell membrane was essentially the same on cells from the antigenic strain and the congeneic control strain, and was about 200-fold less than on the labeled pancreatic duct epithelial cell lateral membranes. Pancreatic beta-cells are therefore one of six known epithelial cell types on which H-2 antigens can not be detected by immunoferritin labeling. The apparent absence of H-2 antigens from these cells suggests a study of the viability of beta-cells in allografts of dissociated islet cells, in which the beta-cell would not be in contact with antigenic cells. Such studies might lead to a new approach to the control of diabetes mellitus by transplantation.


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