Identification of sugar moieties in chief cells of the rat fundic gastric glands

Author(s):  
Laura Gómez-Santos ◽  
Edurne Alonso ◽  
Olatz Crende ◽  
Gaskon Ibarretxe ◽  
Juan Francisco Madrid ◽  
...  
Keyword(s):  
2019 ◽  
Vol 16 (2) ◽  
pp. 0281
Author(s):  
AL –Nakeeb Et al.

          A histological study showed the wall of the stomach in Pica pica and Herpestes javanicus consists of four layers: mucosa, submucosa, muscularis externa and serosa. Also, the present study showed many  differences in the histological structures of the stomach for each in both types. The stomach of P. pica consists of two portions: the proventiculus and gizzard, while the stomach of H. javanicus consists of three portions: cardiac, fundic and pyloric regions. The mucosa layer formed short gastric folds, named plicae. In the proventiculus of P. pica, sulcus is found between each two plicae, but the folds called gastric pits in the gizzard, which are full with koilin. Lamina properia in both types contained gastric glands (straight simple tubular glands) named superficial glands, as well as another gastric gland found in the submucosa layer of the proventiculus in P. pica only named deep gastric glands. The gastric gland in the stomach of H. javanicus contained: mucous neck cells and parietal cells positive to AB/PAS stains in cardiac portion, as well as chief cells in fundic portion, but pyloric portion had just mucous neck cells. Muscularis externa in both types formed two muscle layers: inner and outer layer.


2005 ◽  
Vol 289 (3) ◽  
pp. G521-G529 ◽  
Author(s):  
Guofeng Xie ◽  
Cinthia Drachenberg ◽  
Masahisa Yamada ◽  
Jürgen Wess ◽  
Jean-Pierre Raufman

Muscarinic cholinergic mechanisms play a key role in stimulating gastric pepsinogen secretion. Studies using antagonists suggested that the M3 receptor subtype (M3R) plays a prominent role in mediating pepsinogen secretion, but in situ hybridization indicated expression of M1 receptor (M1R) in rat chief cells. We used mice that were deficient in either the M1 (M1R−/−) or M3 (M3R−/−) receptor or that lacked both receptors (M1/3R−/−) to determine the role of M1R and M3R in mediating cholinergic agonist-induced pepsinogen secretion. Pepsinogen secretion from murine gastric glands was determined by adapting methods used for rabbit and rat stomach. In wild-type (WT) mice, maximal concentrations of carbachol and CCK caused a 3.0- and 2.5-fold increase in pepsinogen secretion, respectively. Maximal carbachol-induced secretion from M1R−/− mouse gastric glands was decreased by 25%. In contrast, there was only a slight decrease in carbachol potency and no change in efficacy when comparing M3R−/− with WT glands. To explore the possibility that both M1R and M3R are involved in carbachol-mediated pepsinogen secretion, we examined secretion from glands prepared from M1/3R−/− double-knockout mice. Strikingly, carbachol-induced pepsinogen secretion was nearly abolished in glands from M1/3R−/− mice, whereas CCK-induced secretion was not altered. In situ hybridization for murine M1R and M3R mRNA in gastric mucosa from WT mice revealed abundant signals for both receptor subtypes in the cytoplasm of chief cells. These data clearly indicate that, in gastric chief cells, a mixture of M1 and M3 receptors mediates cholinergic stimulation of pepsinogen secretion and that no other muscarinic receptor subtypes are involved in this activity. The development of a murine secretory model facilitates use of transgenic mice to investigate the regulation of pepsinogen secretion.


1997 ◽  
Vol 272 (1) ◽  
pp. C48-C58 ◽  
Author(s):  
S. J. Hagen ◽  
S. Takahashi ◽  
R. Jansons

The effect of vacuolation on survival of gastric epithelial cells was studied in rabbit gastric glands (RGG) incubated with ammonia and bafilomycin A1, a potent inhibitor of vacuolar ATPase activity. In ammonia, large vacuoles formed and cell survival was reduced to 47.2 +/- 3.4% at 6 h (59.5 +/- 3.8%, buffer). Bafilomycin A1 added at the start to RGG incubated with ammonia inhibited vacuole formation but did not improve cell survival (48.7 +/- 2.8% at 6 h). Bafilomycin A1 added 1-2 h after addition of ammonia reduced the size of vacuoles but did not alter cell survival. Cell survival was not affected by inhibiting protein synthesis. When incubated with ammonia, parietal cells dissociated from the gland and ruptured. After this, chief cells condensed and formed expensive blebs that contained fragmented nuclei. We conclude that 1)ammonia-induced vacuolation of gastric epithelial cells does not influence cell survival, 2) ammonia facilitates necrosis in parietal cells and apoptosis in chief cells, and 3) chief cell survival, in some manner, may be dependent on parietal cells.


1992 ◽  
Vol 262 (6) ◽  
pp. G1113-G1120
Author(s):  
C. W. Lin ◽  
B. R. Bianchi ◽  
T. R. Miller ◽  
D. G. Witte ◽  
C. A. Wolfram

We evaluated the affinity of cholecystokinin octapeptide (CCK-8), gastrin, and subtype-selective CCK agonists for CCK/gastrin receptors and compared it with the ability of these peptides to stimulate phosphoinositide (PI) hydrolysis and pepsinogen release in guinea pig gastric glands. Competitive binding studies using 125I-labeled Bolton-Hunter-CCK-8 and 125I-gastrin showed the presence of CCK-B/gastrin receptors in gastric glands and dispersed chief cells. In contrast, the potency of peptides in stimulating PI hydrolysis in both gastric glands and dispersed chief cells displayed a profile similar to CCK-A receptors found in pancreatic acini, i.e., CCK-8 = A 71378 greater than A 71623 greater than A 70874 much greater than A 72962 = CCK-8 (desulfated) greater than gastrin II greater than gastrin I. In general, the rank order of potency of peptides for stimulation of PI hydrolysis correlated well with their ability to stimulate pepsinogen release. At concentrations greater than 10 microM, efficacies of gastrin I and II in stimulating pepsinogen release from gastric glands were near 90% of the maximal activity of CCK-8. The inhibitory potency of MK-329, a selective CCK-A receptor antagonist, was similar against either CCK-8 (10 nM) or gastrin I (10 microM), except that a minor portion (approximately 30-40%) of gastrin I-induced pepsinogen release was insensitive to MK-329. The MK-329-insensitive component was inhibited by CI-988, a potent and selective CCK-B/gastrin receptor antagonist.(ABSTRACT TRUNCATED AT 250 WORDS)


2017 ◽  
Vol 49 (6) ◽  
pp. 746-750 ◽  
Author(s):  
Laura Gómez-Santos ◽  
Edurne Alonso ◽  
Lucio Díaz-Flores ◽  
Juan Francisco Madrid ◽  
Francisco José Sáez

1989 ◽  
Vol 23 (1) ◽  
pp. 21-29 ◽  
Author(s):  
N. G. Ghoshal ◽  
H. S. Bal

Histomorphology of the stomach of mouse, rat, hamster, guineapig, gerbil, and rabbit was studied. Although a common structural basis existed in the stomach between these species, the occurrence and distribution of various cells in gastric glands differed considerably between them. In mice, rats, hamsters and gerbils, the lower one-third of the glandular lamina propria was seemingly occupied by a varying proportion of parietal and chief cells. In rabbits, the predominantly occurring chief cells were distributed in the lower three-quarters of the glands intermingling with parietal cells, but in guineapigs the chief cells were not discernible. In hamsters, there was, however, a gradual increase of chief cells from the junction between nonglandular-glandular stomach toward the pyloric region. In all these species, parietal cells were the predominant cell type in the upper half to upper one-third of the gastric glands, often extending up to the neck of the glands interspersing between mucus neck cells and occasionally between chief cells.


2009 ◽  
Vol 296 (6) ◽  
pp. G1211-G1220 ◽  
Author(s):  
Koji Nozaki ◽  
Victoria Weis ◽  
Timothy C. Wang ◽  
András Falus ◽  
James R. Goldenring

The orderly differentiation of cell lineages within gastric glands is regulated by a complicated interplay of local mucosal growth factors and hormones. Histamine secreted from enterochromaffin-like cells plays an important role in not only stimulated gastric acid secretion but also coordination of intramucosal growth and lineage differentiation. We have examined histidine-decarboxylase (HDC)-deficient mice, which lack endogenous histamine synthesis, to evaluate the influence of histamine on differentiation of fundic mucosal lineages and the development of metaplasia following induction of acute oxyntic atrophy. Stomachs from HDC-deficient mice and wild-type mice were evaluated at 8 wk and 12 mo of age. DMP-777 was administrated orally to 6-wk-old mice for 1 to 14 days. Sections of gastric mucosa were stained with antibodies against Mist1, intrinsic factor, H/K-ATPase, trefoil factor 2 (TFF2), chromogranin A, and Ext1 and for the cell cycle marker phospho-histone H3. HDC-deficient mice at 8 wk of age demonstrated a prominent increase in chief cells expressing Mist1 and intrinsic factor. Importantly Mist1-positive mature chief cells were present in the midgland region as well as at the bases of fundic glands, indicating a premature differentiation of chief cells. Mice dually deficient for both HDC and gastrin showed a normal distribution of chief cells in fundic glands. Treatment of HDC-deficient mice with DMP-777 led to loss of parietal cells and an accelerated and exaggerated emergence of mucous cell metaplasia with the presence of dual intrinsic factor and TFF2-expressing cells throughout the gland length, indicative of the emergence of spasmolytic polypeptide-expressing metaplasia (SPEM) from chief cells. These findings indicate that histamine, in concert with gastrin, regulates the appropriate differentiation of chief cells from mucous neck cells as they migrate toward the bases of fundic glands. Nevertheless, histamine is not required for emergence of SPEM following acute oxyntic atrophy.


1990 ◽  
Vol 1 (3) ◽  
pp. 259-268 ◽  
Author(s):  
P A Negulescu ◽  
A Harootunian ◽  
R Y Tsien ◽  
T E Machen

Regulation of cytosolic free Na (Nai) was measured in isolated rabbit gastric glands with the use of a recently developed fluorescent indicator for sodium, SBFI. Intracellular loading of the indicator was achieved by incubation with an acetoxymethyl ester of the dye. Digital imaging of fluorescence was used to monitor Nai in both acid-secreting parietal cells and enzyme-secreting chief cells within intact glands. In situ calibration of Nai with ionophores indicated that SBFI fluorescence (345/385 nm excitation ratio) could resolve 2 mM changes in Nai and was relatively insensitive to changes in K or pH. Measurements on intact glands showed that basal Nai was 8.5 +/- 2.2 mM in parietal cells and 9.2 +/- 3 mM in chief cells. Estimates of Na influx and efflux were made by measuring rates of Nai change after inactivation or reactivation of the Na/K ATPase in a rapid perfusion system. Na/K ATPase inhibition resulting from the removal of extracellular K (Ko) caused Nai to increase at 3.2 +/- 1.5 mM/min and 3.5 +/- 2.7 mM/min in parietal and chief cells, respectively. Na buffering was found to be negligible. Addition of 5 mM Ko and removal of extracellular Na (Nao) caused Nai to decrease rapidly toward 0 mM Na. By subtracting passive Na efflux under these conditions (the rate at which Nai decreased in Na-free solution containing ouabain), an activation curve (dNai/Nai) for the Na/K ATPase was calculated. The pump demonstrated the greatest sensitivity between 5 and 20 mM Nai. At 37 degrees C the pump rate was less than 3 mM/min at 5 mM Nai and 26 mM/min at 25 mM Nai, indicating that the pump has a great ability to respond to changes in Nai in this range. Carbachol, which stimulates secretion from both cell types, was found to stimulate Na influx in both cell types, but did not have detectable effects on Na efflux. dbcAMP+IBMX, potent stimulants of acid secretion, had no effect on Na metabolism.


1984 ◽  
Vol 247 (1) ◽  
pp. G95-G104 ◽  
Author(s):  
J. P. Raufman ◽  
V. E. Sutliff ◽  
D. K. Kasbekar ◽  
R. T. Jensen ◽  
J. D. Gardner

In the present study we examined the actions of various secretagogues on pepsinogen secretion from freshly dispersed chief cells prepared from guinea pig stomach. Chief cells were obtained by preparing dispersed gastric glands, subjecting the glands to mechanical disruption in the presence of EGTA, and fractionating the resulting mucosal cells on a Percoll density gradient. Chief cells constituted 90% of the final cell suspension and cell viability was 99%. In these cells, pepsinogen secretion was stimulated by agents whose actions are probably mediated by calcium: carbachol, cholecystokinin, and A23187. Pepsinogen secretion was also stimulated by agents whose actions are probably mediated by cAMP: secretin, vasoactive intestinal peptide, and 8-bromo-cAMP. Reducing the incubation temperature from 37 degrees to 4 degrees C or adding carbonyl cyanide m-chlorophenylhydrazone abolished secretagogue-induced pepsinogen secretion. These results indicate that freshly dispersed chief cells from guinea pig stomach are responsive to secretagogues and provide a suitable model for investigating cellular mechanisms of secretagogue-induced pepsinogen secretion.


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