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At least 19 recordsLinked to original sources
PubMed1977

Effect of extracellular K+ concentration on resting potential, caerulein-induced depolarization and amylase release from mouse pancreatic acinar cells.

Acinar cell membrane potentials and amylase release were measured from in vitro preparations of mouse pancreas. The effect of a 10-fold increase of the extracellular K+ concentration (to 47 mM) was studied on the resting membrane potential and amylase release as well as on the membrane depolarization and amylase release induced by the cholecystokinin-pancreozymin analogue, caerulein. In the presence of atropine (to exclude the effect of a possible release of endogenous acetylcholine), the increased K+ concentrations depolarized the cells from -45 to -20 mV without influencing the rate of the unstimulated release of amylase. Under these conditions, the depolarizing effect of caerulein was almost abolished, while the caerulein-induced amylase was not. It is concluded that caerulein-induced enzyme secretion from pancreatic acinar cells is independent of the level of the membrane potential as well as extracellular K+ concentration in the range from 4.7--47 mM.

Amylases↗
PubMed1981

Identification and characterization of receptors for secretagogues on pancreatic acinar cells.

Acinar cells from guinea pig pancreas possess six different classes of receptors that mediate the actions of various secretagogues on enzyme secretion. Four classes of receptors stimulate enzyme secretion by causing mobilization of adenylate cyclase and increased cellular cyclic AMP. This paper summarizes the results of studies that have employed radiolabeled secretagogues of high specific activity and have measured directly the interaction of secretagogues with their receptors on pancreatic acinar cells.

Animals↗
PubMed1987

Induction of cells with acinar cell phenotype including presence of intracellular amylase. Treatment with 12-O-tetradecanoyl-phorbol-13-acetate in a neoplastic human salivary intercalated duct cell line grown in athymic nude mice.

The adenocarcinoma produced by transplantation into nude mice of a neoplastic human salivary intercalated duct cell line was treated with 0.1 ml of minimal essential medium (MEM) containing 12-O-tetradecanoyl-phorbol-13-acetate (TPA) at a final concentration of 10(-7) mol/l daily for 28 days and examined morphologically and immunohistochemically. The TPA treatment resulted in an enhancement of tumor growth. In addition, tumor cells containing secretory granules positively reactive to antiamylase serum were observed in the treated tumors, but not in untreated controls. These findings lead us to suggest that neoplastic intercalated duct cells treated with TPA can be induced to differentiate into acinar cells in heterotransplanted athymic nude mice.

Adenocarcinoma↗
PubMed1987

Defective cytoplasmic granule formation. I. Abnormalities affecting tissue mast cells and pancreatic acinar cells of beige mice.

Beige mice (C57BL/6-bgJ/bgJ) express the Chediak-Higashi syndrome, a genetically determined constellation of morphologic and functional abnormalities affecting cells that synthesize cytoplasmic granules; a similar disorder also occurs in humans and several other mammalian species. We used a computer-assisted morphometric approach to identify and quantitate the effect of the beige mutation on the structure of mast cell or pancreatic acinar cell cytoplasmic granules. Beige and control mouse mast cell or pancreatic acinar cell granules exhibited periodic, multimodal distributions of equivalent volumes in which the modes fell at volumes that were integral multiples of the volume of the "unit granule," whose volume (the "unit volume" or v1) was defined by the first mode in the granule equivalent volume distribution. But the modal frequency of the C57BL/6-bgJ/bgJ mast cell granule equivalent volume distribution fell at v1, a pattern consistent with a haphazard pattern of "unit granule" fusion, whereas the corresponding modal frequency for the control mast cell granules fell at v3, a pattern consistent with a "unit addition" model of granule fusion. In addition, the unit volume of beige mouse mast cell granules was 18 times that of control mouse mast cell granules. By contrast, the unit volume of beige mouse pancreatic acinar cell granules was only slightly (23%) greater than that of control cells. C57BL/6-bgJ/bgJ and control cells did not differ significantly in total cell or nuclear volume, or in the aggregate volume of their cytoplasmic granules. However, C57BL/6-bgJ/bgJ mast cells or pancreatic acinar cells contained significantly fewer granules than did their normal counterparts. These findings are consistent with the hypothesis that the beige mutation affects the formation of unit granules and also alters the pattern of aggregation and fusion of unit granules. The data also identify quantitative differences in the expression of the beige mutation in mast cells and pancreatic acinar cells.

Animals↗
PubMed1988

Effects of pancreatic acinar cell surface antibodies and complement on isolated rat acinar cells in vitro.

Surface directed pancreatic acinar cell antibodies raised by immunization of rabbits with suspensions of viable isolated rat acinar cells were utilized to study immune cytolytic processes as a model of in vitro pancreatic injury. The antibodies produced were bound to rat pancreatic acinar cell surface determinants and significantly damaged freshly separated acinar cells by immune cytolytic mechanisms. Addition of complement accelerated the cytolytic effects on the target cells in a dose-dependent manner. The decline of acinar cells was dependent only on the presence of the immune cytolytic potential and not on the number of already damaged cells. Morphologic changes in the cells induced by the agents applied were revealed by both transmission and scanning electron microscopy. The presented experimental model seems a valuable tool for further investigations at the cellular level into the contribution of primarily occurring acinar cell injury in triggering the subsequent pathophysiological mechanisms initiating autodigestion of the pancreatic gland in the pathogenesis of acute pancreatitis.

Animals↗
PubMed1984

A patch-clamp study of potassium channels and whole-cell currents in acinar cells of the mouse lacrimal gland.

Individual acinar cells were isolated enzymatically from the mouse exorbital lacrimal gland. Their electrical characteristics were studied by the patch-clamp methods of single-channel and whole-cell recording as described by Hamill, Marty, Neher, Sakmann & Sigworth (1981). Recording from cell-attached and excised inside-out patches of acinar membrane with quasi-physiological ion gradients demonstrated large outward current events that correspond to single-channel openings. The amplitude, frequency and duration of channel events increased as the membrane patch was depolarized and were reduced by hyperpolarization of the patch membrane. The reversal potential for these channel events is more negative than -40 mV. In excised inside-out patches exposed to quasi-physiological ion gradients single-channel events were abolished when K+ was replaced by Rb+. Since there was no Cl- gradient the channel is clearly highly selective for K+. In excised inside-out patches, when the free Ca2+ concentration bathing the physiological inside of the membrane was raised from less than 10(-9) M to 10(-8) M the frequency and duration of opening of the K+ channel was increased. The channel was almost continuously open when the membrane was exposed to 10(-7) M-free Ca2+. 'Whole cell' recording of lacrimal acinar cells containing 140 mM-KCl and 1 mM-EGTA (with no added Ca2+) provided cell resting membrane potentials of -30 to -40 mV. Depolarizing voltage jumps from the resting membrane potential evoked large outward currents. Hyperpolarizing voltage jumps only evoked small inward currents. Whole-cell recording where RbCl replaced KCl in the pipette provided resting membrane potentials of -20 to -30 mV, reduced the amplitude of outward currents evoked by cell-depolarizing voltage steps by 60% and slowed the time course of the currents. Isolated cells containing 140 mM-KCl and 1 mM-EGTA were voltage clamped at their resting membrane potentials. Acetylcholine (ACh) was applied locally and immediately evoked a strong outward current which rapidly declined to a steady-state level. Sustained agonist responses were obtained by exposing the isolated cell to a solution containing 10(-6) M-ACh. In both K+- and Rb+-filled cells, where the intracellular Ca2+ concentration was buffered by the inclusion of 1 mM-EGTA, 10(-6) M-ACh evoked sustained outward currents that corresponded to cell hyperpolarizations of 5-15 and 10-20 mV, respectively. Increasing intracellular Ca2+ buffering by including 10 mM-EGTA abolished secretagogue-induced outward current in both K+- and Rb+-filled cells. It is concluded that the lacrimal acinar cell membrane contains voltage- and Ca2+-activated K+ channels.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1984

5-Hydroxytryptamine synthesis, storage, and secretion from rat pancreatic acinar cells.

Pancreatic acinar cells are known to synthesize serotonin and dopamine from extracellular precursors. In this study, we found that small amounts of serotonin, alone, were preferentially stored in zymogen granules of acinar cells. Serotonin was apparently incorporated into mature rather than newly formed granules. This was based on the fact that the amine, rather than the newly synthesized zymogen protein, appeared first in the purified granule fraction; additionally, concentrations of cycloheximide, which markedly inhibited de novo synthesis of zymogen protein, did not affect the incorporation of serotonin into the granule fraction. Serotonin, synthesized by the acinar cells, can be secreted along with amylase in a time- and concentration-dependent manner following stimulation of acinar cells by a variety of pancreatic secretagogues. Whether serotonin secreted into pancreatic juice has a biological function remains unknown.

Amylases↗
PubMed1988

BAY-K-8644-stimulated amylase secretion from pancreatic acinar cells.

Pancreatic acinar cells do not contain depolarization-sensitive calcium channels. Nonetheless, in the current study, the calcium channel activator, BAY-K-8644, was found to stimulate a time- and concentration-dependent increase in the spontaneous release of amylase. Secretion was dependent on the presence of extracellular calcium in the incubation medium. Racemic BAY-K-8644 and (or) its S(-)optical isomer did not enhance the secretory response to either carbachol or cholecystokinin octapeptide; however, when co-applied with either phorbol ester, vasoactive intestinal peptide, or forskolin, they potentiated amylase secretion. Nifedipine and the R(+)isomer of BAY-K-8644, which are both calcium channel antagonists, did not alter basal or forskolin-stimulated amylase secretion, and [3H]nitrendipine did not bind to acinar cell membranes. Neither atropine nor dibutyryl cGMP, inhibitors of cholinergic and cholecystokininergic receptors, respectively, affected BAY-K-8644-induced amylase secretion. While BAY-K-8644 stimulated concentration-dependent cGMP synthesis in acinar cells, it had no effect on basal or forskolin-stimulated cAMP formation. The data suggest that BAY-K-8644 may bind to acinar cell sites that are not functional calcium channel proteins but are coupled nevertheless to the secretory response, and that calcium channel antagonists do not bind to these sites. The mechanism of the secretagogue action of BAY-K-8644 remains to be elucidated.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1979

Effect of CCK-octapeptide and secretin on amylase secretion in isolated rat pancreatic acinar cells.

Isolated acinar cells from rat pancreas responded well to hormonal treatment. Both secretin (synthetic and highly purified from porcine origin) and CCK-octapeptide stimulated amylase secretion in these cells. The response in both cases was very rapid. A maximal output of enzyme was reached within 5-10 min after the addition of hormones. The concentration producing maximal output for synthetic secretin (Schwarz/Mann) was 5 x 10(-8) M, synthetic secretin (Squibb), 10(-5) M, for purified porcine secretin, 10(-5) M, and for CCK-octapeptide was 5 x 10(-10) M. Secretin (2-fold at optimal concentration) was found to be less efficient compared to CCK-octapeptide (5-fold at optimal concentration) in stimulating amylase release. A combination of secretin and CCK-octapeptide had a synergistic action in stimulating enzyme release by the acinar cells. In addition, pretreatment of acinar cells with secretin potentiated the secretory response of the treated cells to CCK-octapeptide. To a lesser extent pretreatment with CCK-octapeptide also increased the effect of secretin in stimulating enzyme secretion.

Amylases↗
PubMed1976

Effects of ions on amylase release by dissociated pancreatic acinar cells.

Dissociated acinar cells prepared from guinea pig and mouse pancreas were intact on the basis of structure, ion content, and their ability to increase release of amylase in response to bethanechol and the calcium ionophore A23187. Guinea pig but not mouse acinar cells increased amylase release in response to caerulein. An increase in the concentration of K+ in the medium, which increases amylase release from whole pancreas, did not increase release. The effect of varying the ionic content of the medium on basal and stimulated amylase release was studied. Bethanechol and caerulein were still able to stimulate amylase release when Ca2+ was omitted from the medium, whereas stimulation induced by A23187 was abolished. Elevation of the concentration of Mg2+ did not affect basal or stimulated amylase release. Removal of Na+ from the medium initially had no effect on amylase release although bethanechol-stimulated release by mouse cells was inion of the HCO3- or Cl- content of the medium did not affect cholinergic stimulation of secretion. It is concluded that stimulated amylase release by isolated acinar cells is relatively independent of the ionic constituency of the bathing medium.

Amylases↗
PubMed1989

Density gradient separation of two populations of lysosomes from rat parotid acinar cells.

Exocrine acinar cells possess two cytochemically distinct populations of secondary lysosomes. One population is Golgi associated and has demonstrable acid phosphatase (AcPase) activity, whereas the second is basally located and lacks AcPase activity but has trimetaphosphatase (TMPase) activity. The basal lysosomes are tubular in shape and rapidly label with horseradish peroxidase (HRP) after intravenous injection. In the present study using isolated rat parotid acinar cells, the two lysosomal populations were separated by cell fractionation on Percoll density gradients and were analyzed biochemically and by EM cytochemistry. On 35% Percoll gradients, two peaks of AcPase and beta-hexosaminidase, both lysosomal marker enzymes, and succinic dehydrogenase, an enzyme marker for mitochondria, could be resolved. The major peaks of beta-hexosaminidase and succinic dehydrogenase and the minor peak of AcPase corresponded with the dense lysosome fraction. The major peak of AcPase and the minor peaks for beta-hexosaminidase and succinic dehydrogenase coincided with the light membrane fraction. Galactosyl transferase (a marker enzyme for Golgi saccules) and 5'-nucleotidase (a plasma membrane marker) were also associated with this fraction. By electron microscopy, the light membrane fraction was seen to contain tubular elements, multivesicular bodies (MVB), Golgi saccules, GERL, immature secretory granules, and some mitochondria. Electron microscopic cytochemical examination showed that these tubular structures were lysosomes. The dense lysosome fraction contained lysosomes positive for both AcPase and TMPase. After continuous incubation of isolated acinar cells with HRP, reaction product was rapidly localized to the light membrane fraction (greater than 2 min), where it was found in vesicles and tubular lysosomes. By 10 min it was present in MVB and tubular lysosomes, but by 60 min no HRP reaction product had appeared in the dense lysosomes. These results demonstrate that the tubular lysosomes are separable from dense lysosomes, typical secondary lysosomes, and are involved in the initial stages of endocytosis.

Acid Anhydride Hydrolases↗
PubMed1989

Epidermal growth factor inhibits rat pancreatic cell proliferation, causes acinar cell hypertrophy, and prevents caerulein-induced desensitization of amylase release.

The in vivo effects of epidermal growth factor (EGF) on pancreatic growth and digestive enzyme concentrations were compared with the actions of the pancreatic secretagogue caerulein in the adult rat. EGF (10 micrograms/kg BW) did not alter pancreatic weight or protein content. However, this concentration of EGF inhibited [3H]thymidine incorporation into DNA by 44%, decreased DNA content by 20%, and increased the concentrations of amylase, chymotrypsinogen, and protein by 106%, 232%, and 42%, respectively. Pancreatic acini prepared from EGF-treated rats exhibited a characteristic secretory response to caerulein that was superimposable to that obtained in acini from saline-treated rats. In both groups of acini half-maximal and maximal stimulation of amylase release occurred at approximately 5 pM and 50 pM caerulein, respectively. In contrast to EGF, caerulein (1 microgram/kg BW) increased pancreatic weight by 29% and protein content by 59%, and enhanced [3H]thymidine incorporation into DNA by 70%. Although caerulein increased the concentrations of pancreatic amylase and chymotrypsinogen by 38% and 297%, respectively, pancreatic acini prepared from caerulein-treated rats were less sensitive to the actions of caerulein in vitro when compared with acini from control rats. Indeed, the EC50 was shift from 4.8 pM to 9.8 pM after 4 days of treatment. EGF potentiated the actions of caerulein on pancreatic weight, protein content, and chymotrypsinogen concentration, and prevented the caerulein-induced alteration in the secretory responsiveness of the acinar cell. Conversely, caerulein reversed the inhibitory effect of EGF on thymidine incorporation. These findings suggest that EGF may modulate the trophic effects of certain gastrointestinal hormones, and may participate in the regulation of pancreatic exocrine function in vivo.

Amylases↗
PubMed1991

Oscillations of cytosolic sodium during calcium oscillations in exocrine acinar cells.

In acinar cells from rat salivary glands, cholinergic agonists cause oscillations in cytoplasmic free calcium concentration, which then drive oscillations of cell volume that reflect oscillating cell solute content and fluid secretion. By quantitative fluorescence ratio microscopy of an intracellular indicator dye for sodium, it has now been shown that large amplitude oscillations of sodium concentration were associated with the calcium and cell volume oscillations. Both calcium and sodium oscillations were dependent on the continued presence of calcium in the extracellular medium and were abolished by the specific sodium-potassium adenosine triphosphatase inhibitor ouabain. Thus, calcium oscillations in salivary acinar cells, by modulating the activities of ion transport pathways in the plasma membrane, can cause significant oscillations of monovalent ions that may in turn feed back to regulate calcium oscillations and fluid secretion.

Animals↗
PubMed1977

Development of acinar cells in the rat submandibular gland.

Three types of cells - terminal tubule cells, proacinar cells and acinar cells - have been observed during the development of acini in the rat submandibular gland. The terminal tubules are lined by terminal tubule cells which show PAS-positive, dark granules. From the terminal tubules pouches develop which are lined by similar cells to those lining the terminal tubules. These pouches give rise to the next generation of terminal tubules. The last generation of terminal tubules, whose cells lose their dark, PAS-positive granules, develop into secondary tubules lined by proacinar cells. At 14 days of age large coarse granules appear in the cytoplasm of the proacinar cells lining the secondary tubules as well as in the cells of intercalated ducts. These granules are discharged into the lumen of the tubule and the proacinar cells become foamy-looking acinar cells, while the secondary tubule becomes an acinus. Thus the terminal tubule cells give rise to proacinar cells which become acinar cells and cells to the intercalated duct cells. The development of acini in the rat submandibular gland thus takes place in three stages: (1) development of terminal tubules by continuing pouch formation up to 12 days of age, (2) conversion of terminal tubules into secondary tubules tined by proacinar cells from 6 to 12 days of age, and (3) development of large coarse granules in proacinar cells and their excretion into the lumen of tubules, resulting in the transformation of proacinar cells into acinar cells between 14 and 21 days.

Age Factors↗
PubMed1983

Characterization of basal lysosomes in exocrine acinar cells.

Exocrine acinar cells possess a unique system of basally located lysosomes. Cytochemically, these lysosomes do not contain acid phosphatase, but react positively for trimetaphosphatase (C Oliver: J Histochem Cytochem 28:78, 1980). The present study extends the morphological and cytochemical characterization of these lysosomes in pancreatic, parotid, and exorbital lacrimal acinar cells from Sprague-Dawley rats and National Institutes of Health Swiss mice. The basal lysosomes are highly pleomoric in nature, and frequently appear as a system of anastomosing tubules of varying width. The lysosomes have a close morphological relationship with both the rough endoplasmic reticulum and mitochondria. In addition to trimetaphosphatase activity, the lysosomes are reactive for aryl sulfatase B, thiolacetic acid esterase, and cholinesterase. Since the cholinesterase activity could not be inhibited by specific inhibitors, this activity is most likely due to the presence of nonspecific esterases. The results of this study confirm the lysosomal nature of the basal lysosomes and underscore the necessity of using multiple enzyme activities to identify and characterize lysosomes.

Acid Anhydride Hydrolases↗
PubMed1985

Activation of Ca2+-dependent Cl- and K+ conductances in rat and mouse parotid acinar cells.

Isolated acinar cells from rat and mouse parotid glands were studied with patch-clamp whole-cell current recordings. Acetylcholine (ACh) stimulation caused a transient inward current at a membrane potential of -70 mV, and a sustained outward current at a membrane potential of 0 mV, in quasi physiological Na+, K+ ion gradients, except the zero-Cl- ion gradient condition across the membrane. The reversal potential obtained from the ACh-evoked steady current was about -75 mV, in this ionic condition. When major Cl- ions of both the pipette and the bath solution were replaced, either by glutamate or by sulphate, only a large outward current was observed, at a membrane potential of -60 mV, in the presence of ACh. The addition of Ca2+-ionophore A23187 caused responses similar to those evoked by ACh. The reversal potential of A23187-induced current was close to the K+ equilibrium potential of -90 mV, in a Cl- -free condition. When K+-free NaCl solution was used in the pipette and the bath, A23187 caused only a large inward current, at a membrane potential of -60 mV. The reversal potential of A23187-evoked current was about -15 mV, in a symmetrical K+-free, NaCl condition. These results suggest that the ACh and A23187 activate Cl- as well as K+ conducting pathways via an increase in [Ca2+]i in the parotid acinar cells. The A23187-evoked large K+ current could not be explained solely by a rise in open probability of the channels.

Acetylcholine↗
PubMed1977

Exocrine pancreas under experimental conditions. III. Membrane and cell junctions in isolated acinar cells.

The ultrastructure of the cell membrane and intercellular junctions was studied after isolation of exocrine pancreatic cells by tryptic digestion and mechanical treatment. The number and distribution of membrane associated particles does not change significantly when acinar cells in situ are compared to those after the isolation procedure. However, intercellular junctions undergo distinct alterations. Gap junctions in normal pancreatic cells are macular in shape and localized at the lateral parts of the cell membrane. In isolated acinar cells gap junctions are irregularly shaped, more extended, and frequently associated with tight junctions. Tight junctions form belt-like structures which are found to persist after isolation but subsequently become elongated and interrupted. Thus extensive macular areas of tight junctions develop. Further, the strands on the P-face and the grooves on the E-face of freeze-fracture replicas change in array, dissociate, and become loosely packed on large membrane areas. The present investigation shows that the intramembranous proteins of tight and gap junctions are mobile structures within the fluid membrane. The shape of their array is dependent on the form of the intercellular contact zone.

Animals↗
PubMed1991

Secretagogue induction of cell differentiation in pancreatic acinar cells in vitro.

The effect of two different types of secretagogues on rat pancreatic acinar cells cultured onto a reconstituted basement membrane was studied. Cells cultured without any secretagogue were able to reaggregate but did not form monolayer patches. Most of them lost their differentiated ultrastructural characteristics but regained their polarity. In contrast, when CCK, caerulein, or carbamylcholine was added to the culture medium cells developed both acini-like structures and cell monolayer patches. The cells retained the differentiated ultrastructural appearance and polarity resembling their in situ morphology. Furthermore, secretagogue-conditioned cells presented higher amylase contents. The use of secretagogue antagonists such as L-364,718 and L-365,260 for caerulein, or atropine and mecamylamine for carbamylcholine, did not profoundly modify the cultures and the morphological effects triggered by the secretagogues alone. However, both CCK antagonists and cholinergic antagonists inhibited to a certain degree the secretory stimulation. Our data support the theory that a major role is played by secretagogues in conjunction with the basement membrane for the maintenance of differentiation in pancreatic acinar cells in vitro which appears to be independent from their secretory effect.

Amylases↗