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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↗

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↗

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↗

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↗

PubMed2025

GZMK+CD8+ T cells target a specific acinar cell type in Sjögren's disease.

OBJECTIVES: Sjögren's disease (SjD) is a systemic autoimmune disorder characterized by dysfunction of exocrine glands, particularly the salivary and lacrimal glands, with no clear etiology or effective therapy. This study explores the complex interplay of varied cell types in the salivary glands and their role in the pathology of Sjögren's disease. METHODS: Utilizing single-cell and spatial transcriptomics alongside spatial immunophenotyping to analyze human minor salivary glands, we developed a comprehensive understanding of the cellular landscape of non-SjD salivary glands and how that landscape changes in SjD patients. In vitro cellular assays and novel patient-derived primary epithelial cells were co-cultured with autologous T cells to confirm effector states and the delivery and effect of disease-associated granzymes. RESULTS: We identified previously unrecognized heterogeneity among acinar cells, including a PRR4⁺CST3⁺WFDC2⁻ seromucous acinar population that is selectively lost in Sjögren's disease. Expression and organizational changes were linked to clinical features: (i) T cells in the glands of SSA⁺, high-focus score patients showed increased transcriptional signatures of activation, antigen presentation, and apoptosis resistance compared with patients with mild or moderate disease, and (ii) patients with low immune infiltration exhibited distinct epithelial organization. Notably, GZMK⁺CD8⁺ T cells, which accumulate with disease severity, displayed a cytotoxic transcriptional program, degranulated upon stimulation ex vivo, and localized spatially with immune-engaged epithelial cells. Functional assays demonstrated that GZMK activates interferon signaling in vitro, and autologous co-cultures of patient-derived T cells and epithelial cells validated these findings. CONCLUSIONS: Using single-cell and spatial transcriptomics and proteomics, this study identifies a selective loss of PRR4⁺CST3⁺WFDC2⁻ seromucous acinar cells and a rise in GZMK⁺CD8⁺ T cells in Sjögren's disease, revealing distinct immune-mediated epithelial remodeling and interferon-driven dysfunction across diverse clinical presentations. These findings uncover a novel sub-cytolytic effector mechanism by which GZMK⁺CD8⁺ T cells impair mitochondrial integrity and activate innate immune signaling, linking epithelial injury to type I interferon responses and offering new therapeutic targets.

Humans↗

PubMed1978

Effects of calcium and chelating agents on the ability of various agonists to increase cyclic GMP in pancreatic acinar cells.

In dispersed acinar cells from guinea pig pancreas we found that chelating extracellular calcium with EDTA did not alter cellular cyclic GMP but caused a 50% reduction in the increase in cyclic GMP caused by the synthetic C-terminal octapeptide of porcine cholecystokinin (cholecystokinin octapeptide). This effect was maximal within 2 min and preincubating the cells with EDTA for as long as 30 min caused no further reduction in the action of cholecystokinin octapeptide. In acinar cells preincubated without calcium, adding calcium caused a time dependent increase in the action of cholecystokinin octapeptide and this increase was maximal after 10 min of incubation. An effect of extracellular calcium on the action of cholecystokinin octapeptide could be detected with 0.5 mM calcium and was maximal with 2.0 mM calcium. Magnesium alone or with calcium did not alter the action of cholecystokinin octapeptide. Extracellular calcium did not alter the time course or the configuration of the dose vs. response curve for the action of cholecystokinin octapeptide on cellular cyclic GMP. Low concentrations of EGTA (0.1 mM) decreased the effect of cholecystokinin octapeptide on cellular cyclic GMP to the same extent as did EDTA or preincubating acinar cells without calcium. Increasing EGTA above 0.1 mM caused progressive augmentation of the action of cholecystokinin octapeptide on cellular cyclic GMP and this augmentation did not require extracellular calcium or magnesium. Results similar to those obtained with cholecystokinin octapeptide were also obtained with bombesin, carbamylcholine, litorin and eledoisin. In contrast, the action of sodium nitroprusside on cyclic GMP in pancreatic acinar cells was not altered by adding EDTA or EGTA. These results indicate that the ability of extracellular calcium to influence the action of cholecystokinin octapeptide and other agents on cyclic GMP results from changes in cellular calcium and not from effects of extracellular calcium per se. The action of low concentrations of EGTA on the increase in cyclic GMP caused by various agents reflects the ability of EGTA to chelate extracellular calcium. The actions of high concentrations of EGTA were independent of extracellular calcium or magnesium and appear to reflect a direct action of EGTA on pancreatic acinar cells.

Animals↗

PubMed1978

Actions of peptides isolated from amphibian skin on pancreatic acinar cells.

In dispersed acinar cells prepared from guinea pig pancreas, peptides isolated from amphibian skin (caerulein, bombesin, litorin, and physalaemin) as well as eledoisin, a peptide isolated from the posterior salivary gland of a Mediterranean octopod, increased outflux of 45Ca, release of bound 45Ca, accumulation of cyclic GMP, and release of amylase. In addition, bombesin, litorin, physalaemin, and eledoisin each increased the initial uptake of 45Ca by dispersed acinar cells, whereas C-terminal octapeptide of porcine cholecystokinin (CCK-OP) and carbamylcholine did not increase the initial uptake of 45Ca but, rather, abolished the increase caused by the other agents. None of the actions of these amphibian peptides was altered by concentrations of atropine sufficient to abolish the effects of muscarinic cholinergic agents. None of the amphibian peptides altered cellular cyclic AMP or the increase caused by secretin or porcine vasoactive intestinal peptide (VIP). Acinar cells preincubated with 45Ca plus bombesin showed the same rate of release of 45Ca as did control cells and this rate was not altered by adding bombesin but was increased fivefold by adding CCK-OP. In terms of their chemical structures as well as the potency and efficacy with which they alter acinar cell function, the amphibian peptides plus CCK-OP can be grouped into three pairs: caerulein with CCK-OP, bombesin with litorin, and physalaemin with eledoisin.

Amylases↗

PubMed1976

Action of cholecystokinin and cholinergic agents on membrane-bound calcium in dispersed pancreatic acinar cells.

In dispersed acinar cells prepared from guinea pig pancreas, cellular uptake of 45Ca was moderately rapid and reached a steady state by 60 min. At the steady state, 69% of total cellular 45Ca was membrane-bound. In acinar cells preloaded with 45Ca and then incubated with COOH-terminal octapeptide of cholecystokinin (CCK-OP) or carbamylcholine, total cellular 45Ca decreased by approximately 40% within 5-10 min and then steadily increased to control values by 60 min. Under identical conditions, membrane-bound 45Ca decreased by 40% within 5-10 min and remained constant for the duration of the incubation. Free cellular 45Ca did not change during the initial 30 min but then increased steadily to values three times those in control cells by 60 min. In cells preloaded with 45Ca and then incubated with EDTA, the loss of total cellular radioactivity stimulated by CCK-OP could be accounted for by loss of membrane-bound 45Ca. CCK-OP failed to alter total cellular uptake of 45Ca when both tracer and peptide were added at the beginning of the incubation. Under identical conditions, membrane-bound 45Ca was not altered by CCK-OP during the first 30 min of incubation but was significantly below control values after this time. The effect of CCK-OP on free cellular 45Ca was the same as in cells preloaded with the tracer. These results suggest that CCK-OP causes release of 45Ca from a membrane-bound compartment that equilibrates slowly with extracellular fluid and that the change in free cellular 45Ca is a secondary effect.

Animals↗

PubMed1977

Foreign serum-induced pancreatitis in mice. II. Secretory disturbances of acinar cells.

As previously reported, pancreatic acinar cell necrosis and inflammation develop in mice a few hours after one intraperitoneal injection of foreign serum. However, sublethally injured acinar cells exhibited notable increases in both zymogen granule numbers and amylase activity, observed within 3 hours and increasing with time. These two changes were coupled with a progressive decrease in the secretory response to pilocarpine and were preceded by significant disturbances in pancreatic tissue concentrations of sodium and potassium. We conclude that (1) the granule increase results from an induced disturbance of the granule exocytosis mechanism while granule formation continues and, therefore, (2) the granule secretory process is more sensitive to the serum injury mechanism than is the zymogen synthesis process. Although the granule increases developed in acinar cells throughout most of the nonnecrotic gland and persisted for at least 24 hours, acinar cell necrosis was maximal in extent--approximately 25% of the gland in severest form--by 12 to 15 hours. We conclude, therefore, that the increase in granules is neither the primary determinant nor initiator of acinar cell death. The latter is likely caused by disturbed plasma membrane functions, sufficient in some cells to result in lethal changes in ion and fluid composition. The injury mechanism, which permits granule formation to go on in the face of impaired granule exocytosis, is yet to be worked out. The possibilities are discussed in relationship to the reactivity of foreign sera for target cell plasma membranes.

Amylases↗

PubMed1977

Scanning electron microscopy of dissociated pancreatic acinar cell surfaces.

The pancreatic acinar cell surfaces have been studied by SEM with a dissection of technique and correlated with results obtained by TEM. The SEM results demonstrate characteristic arrangement of microplicae which in some areas are densely packed. In many areas, the microplicae are distributed in such a manner that they create zones with typical geometrical shapes and show a relatively smooth surface. These smooth areas may coincide, as indicated by correlated TEM results, with the limits of intimate contact between adjacent acinar cells which, in turn, represent part of the junctional complex. Another aspect revealed by these SEM preparations concerns the presence of groups of densely packed microplicae, arranged in regular rows and distributed along some grooves and/or infoldings of the cellular surface. On the basis of SEM and TEM information, it is likely that these structures correspond to intercellular (and possibly, in some cases, intracellular) canaliculi which topographically form a kind of extensive microlabyrinthine arrangement running along all the cell sides. One final point revealed by fractured samples concerns the finding of spherical zymogen droplets within the vesicles of the Golgi complex. Because in many scanning images these vesicles appear connected by small openings, it is suggested that they may represent a system of intercommunicating chambers (vacuoles) through which the zymogen droplets can be continuously accumulated and discharged into the acinar lumen.

Animals↗

PubMed1977

Ultrastructural and functional changes in pancreatic acinar cells during autolysis.

Effects of anoxemic cell injury on rat pancreatic acinar cells were studied in a preparation where tissue samples were incubated at temperature between 18-20 degrees C in a moist atmosphere for 0, 0.5, 1, 3, 6, 12, and 24 h in vitro. Electron microscopy revealed that disintegration of acinar cells began by swelling of various cell compartments and gradual breakdown of cell membranes. Zymogen granules remained morphologically intact for at least 3 h. There were no signs of increased autophagic activity during the period of observation. Myelin figures and other membranous remnants of disintegrated cells, together with individual cells and cell organelles whose morphology was relatively well preserved were seen even after w4 h incubation. The secretory response of acinar cells to pancreozymin stimulation, as measured by amylase release into the incubation medium in vitro, decreased progressively closer to zero during 12 h autolysis. No active trypsin could be detected in the tissue samples during the 24 h observation time. It was concluded that during hypoxic autolysis at room temperature between 18-20 degrees C in vitro: 1. Acinar cell disintegration results from breakdown of cellular membranes, 2. autophagocytosis is not involved, 3. most of zymogen granules remain morphologically intact even at the time when cell membranes show evidence of damage, 4. there is no trypsin activation taking place in the tissue, and 5. the acinar cells are capable of responding to secretory stimulation for 3 to 6 h after removal of the tissue from the experimental animal.

Amylases↗

PubMed1979

Formation and fate of ethionine-induced cytoplasmic crystalloids in rat parotid acinar cells.

The formation and fate of cytoplasmic crystalloids in rat parotid acinar cells were investigated during ethionine intoxication and recovery. By day 3 of ethionine treatment, acinar cells had numerous autophagic vacuoles containing recognizable secretory granules and fragments of rough endoplasmic reticulum. By day 5, immature crystalloids were present in many of the autophagic vacuoles, and as the crystalloids matured, a 7-nm periodicity became apparent. Crystalloids were never observed in the Golgi saccules or in any other organelle associated with secretory granule formation. When ethionine treatment was stopped, the acinar cells rapidly returned to their normal morphology. The majority of the crystalloids and autophagic vacuoles were lost from the cells during the first two to three days of recovery. At this time annulate lamellae were present intracellularly, and macrophages, many containing crystalloids, were associated with the basal surface of the acinar cells. These results indicate that the cytoplasmic crystalloids are formed in autophagic vacuoles, and do not represent an abnormal secretory product. Additiontionally, during recovery crystalloids may be removed from the acinar cells by interaction with macrophages. The sequence of autophagic vacuole formation, development of crystalloids, macrophage infiltration and phagocytosis of acinar cell debris appears to be a non-specific response of the rat parotid gland to cellular injury occurring in a variety of experimental and pathological conditions.

Animals↗

PubMed1979

Pancreatic acinar cells: effects of micro-ionophoretic polypeptide application on membrane potential and resistance.

1. Acinar cell membrane potential and resistance were measured from superfused segments of mouse pancreas, in vitro, using intracellular glass micro-electrodes. One or two extracellular micropipettes containing caerulein, bombesin nonapeptide (Bn) or acetylcholine (ACh) were placed near to the surface of the impaled acinus. The secretagogues were ejected rapidly from the micropipettes by ionophoresis.2. Each secretagogue evoked a similar electrical response from the impaled acinar cell: membrane depolarization and a simultaneous reduction in input resistance. The duration of cell activation from caerulein ionophoresis was longer than that observed for ACh and Bn. The cell response to the peptide hormone applications could be repeated in the presence of atropine.3. The minimum interval before the onset of cell depolarization after caerulein ionophoresis was determined. Values ranged between 500 and 1000 msec. The minimum latencies after Bn ionophoresis were 500-1400 msec.4. With two electrodes inserted into electrically coupled acinar cells, direct measurements of the caerulein and Bn null potentials were made. At high negative membrane potentials an enhanced depolarization was evoked by caerulein ionophoresis. At low negative membrane potentials the caerulein stimulation produced a diminished depolarization, and at membrane potentials less than - 10 mV acinar cell hyperpolarizations were observed. A similar series of responses was obtained in experiments where Bn ionophoresis was used. The caerulein and the Bn null potentials were always contained within - 10 to - 15 mV.5. The results describe the almost identical electrical response of acinar cells to stimulation by ACh, caerulein and bombesin. All three secretagogues have similar null potentials and latencies of activation on acinar cells. The bombesin latency responses appear as short as those measured for caerulein and provide electro-physiological evidence that Bn acts directly on acinar cells. The findings support the hypothesis that ACh, caerulein and Bn, though acting on different receptors, evoke the observed changes in electrical properties of acinar cell membranes, through a common pathway.

Acetylcholine↗

PubMed1978

The interaction of caerulein with the rat pancreas. 2. Specific binding of [3H]caerulein on dispersed acinar cells.

1. [3H]Caerulein was bound to dispersed acinar cells from rat pancreas in a rapid, reversible, specific, saturable, and temperature-dependent manner. Binding decreased above pH 6.5. Treatment of intact cells with 2, 4-dinitrophenol and oligomycin, p-choloromercuribenzoate, diisopropylfluoro-phosphate and glutaraldehyde impaired [3H]caerulein binding whereas the addition of EGTA inhibited binding. The C-terminal octapeptide of pancreozymin, desulfated caerulein and pentagastrin inhibited binding of [3H]caerulein whereas vasoactive intestinal polypeptide, secretin, bombesin or carbamoylcholine were wothout effect. The good resistance of [3H]caerulein to inactivation by acinar cells at 37 degrees C was reflected in the high proportion of tracer remaining capable of binding to fresh acinar cells. 2. Scatchard plots of [3H]caerulein binding were curvilinear with an upward concavity. The addition of an excess of unlabeled caerulein resulted in the release of as much as 65% of bound [3H]caerulein within 1 min at 37 degrees C. The dissociation of remainder followed much slower kinetics. 3. The results suggested that intact rat pancreatic acinar cells have one class of caerulein binding sites existing in two states: one with high affinity and another with low affinity, the proportion of sites in each state depending on the degree of site occupancy (negative cooperativity), and on the intracellular concentration of nucleotides.

Animals↗

PubMed1979

[The three-dimensional ultrastructure of the pancreatic acinar cell (authors transl)].

The pancreatic acinar cells of normal rats were studied by scanning electron microscope. A three-dimensional image is presented of the structure and arrangement of the zymogen granules as well as of the apical microvilli and the zymogen discharge in the pancreatic acinar cell. The study of these structures in physiologic and pathologic conditions by scanning electron microscopy can be recommended to support the understanding of findings obtained by light and transmission electron microscopy.

Animals↗

PubMed1976

Ultrastructures of atypical acinar cell nodules in rat pancreas induced by 4-hydroxyaminoquinoline-1-oxide.

A single intravenous injection of 4-hydroxyaminoquinoline-1-oxide (4HAQO) to rats induces multiple atypical acinar cell nodules in the pancreas. In this study, the ultrastructure of cells in these nodules was examined at 6, 9, and 12 months, and the features were compared to those of developing embryonal pancreas. The cells in the nodules are exocrine acinar cells in type and exhibited several features which distinguish them from the nonnodular acinar cells. Irregular nuclear shape with enlarged nucleoli was frequently observed. Zymogen granules in the nodular cells appeared as vesicles with contents of extreme electrom lucency and their ultrastructural appearance was similar to those of developing embryonic pancreatic acinar cells at 16 and 18 days of gestation. At the cell periphery, the lateral cell membrane showed bizarre interdigitation and the ectoplasm showed hyaloplasmic rarefaction. These findings indicate that the acinar cell nodules induced by 4-hydroxyaminoquinoline-1-oxide are composed of a new population of phenotypically altered acinar cells showing nuclear abnormalities, modified cell to cell interaction, and a possible defect in synthesis and/or maturation of secretory enzymes. The latter may indicate an arrest in the differentiation of acinar cells. The significance of these findings is discusses, and it is suggested that the atypical nodules in the pancreas induced by 4-hydroxyaminoquinoline-1-oxide may represent early neoplastic foci.

4-Hydroxyaminoquinoline-1-oxide↗

PubMed1976

Postnatal development of acinar cells in rat submandibular gland as revealed by electron microscopic staining for carbohydrates.

The postnatal differentiation of acinar cells in rat submandibular gland was studied by staining with periodic acid-thiosemicarbazide-silver proteinate to identify carbohydrate-containing macromolecules in the electron microscope. This method revealed glycogen particles and internal substructure in the secretory granules of developing acinar cells. On the basis of morphologic and histochemical criteria three phases of acinar cell development were defined. In the pro-acinar phase, during the first week after birth, pro-acinar cells and terminal tubular cells were the main components of the terminal tubules in the rudimentary gland. The secretory granules of the pro-acinar cells contained speckled or rod-like substructures which stained intensively for carbohydrates and were digested by proteolytic enzymes. During the second to third week after birth, which is the immature-acinar-cell phase, thread-like substructures were seen in the secretory granules. These structures, which were not digested by proteolytic enzymes, disappeared gradually. The acinar cells of 4-week-old or older rats displayed no particular substructure in the secretion granules and represented the final, mature phase of development.

Age Factors↗