Age-related alterations of gastric mucosa and estrogen synthesis in rat parietal cells

Author(s):  
Hiroto Kobayashi ◽  
Nobuyuki Shirasawa ◽  
Akira Naito
1956 ◽  
Vol 187 (3) ◽  
pp. 427-431 ◽  
Author(s):  
Joseph J. Vitale ◽  
Oscar M. Jankelson ◽  
Patricia Connors ◽  
D. Mark Hegsted ◽  
Norman Zamcheck

Effect of histamine on the activity of succinic oxidase and malic dehydrogenase was studied in guinea pig and human gastric mucosa. Human tissue was obtained through the surgical services of the Boston City Hospital. Control value for the succinic oxidase system of the proximal half of the guinea pig stomach was approximately 480 ( Qo2 (N) (µl O2/mg nitrogen/hr.)). After histamine, this value rose to 550 in 30 minutes with a simultaneous rise in titratable acidity of the stomach contents. Animals fasted for 72 hours had a Qo2 (N) of approximately 500 and after histamine a Qo2 (N) of 700 was observed. Spectrophotometric analysis of succinic dehydrogenase and cytochrome oxidase activities, two of the major components of the succinic oxidase system, revealed that both components are increased following histamine administration. Malic dehydrogenase, however, was not affected by histamine treatment. Succinic dehydrogenase was demonstrated by histochemical localization and was concentrated below the superficial mucous layer where parietal cells were abundant. Succinic oxidase activity of human gastric mucosa was demonstrable only in those specimens containing abundant parietal cells. This study confirms the view that HCl production by parietal cells is associated with aerobic metabolism and is perhaps under enzymatic control. The study suggests that the succinic oxidase system may be involved in the production or secretion of HCl.


1989 ◽  
Vol 256 (1) ◽  
pp. G254-G263 ◽  
Author(s):  
C. S. Chew ◽  
M. Ljungstrom ◽  
A. Smolka ◽  
M. R. Brown

A new procedure for isolation and primary culture of gastric parietal cells is described. Parietal cells from rabbit gastric mucosa are enriched to greater than 95% purity by combining a Nycodenz gradient separation with centrifugal elutriation. Cells are plated on the basement membrane matrix, Matrigel, and maintained in culture for at least 1 wk. Parietal cells cultured in this manner remain differentiated, cross-react with monoclonal H+-K+-ATPase antibodies, and respond to histamine, gastrin, and cholinergic stimulation with increased acid production as measured by accumulation of the weak base, [14C]aminopyrine. When stimulated, cultured cells undergo ultrastructural changes in which intracellular canaliculi expand and numerous microvilli are observed. These ultrastructural changes are similar to those previously found to occur in vivo and in acutely isolated parietal cells. Morphological transformations in living cells can also be observed with differential interference contrast optics in the light microscope. After histamine stimulation, intracellular canaliculi gradually expand to form large vacuolar spaces. When the H2 receptor antagonist, cimetidine, is added to histamine-stimulated cells, these vacuoles gradually disappear. The ability to maintain hormonally responsive parietal cells in primary culture should make it possible to study direct, long-term effects of a variety of agonists and antagonists on parietal cell secretory-related activity. These cultured cells should also prove to be useful for the study of calcium transients, ion fluxes, and intracellular pH as related to acid secretion in single cells, particularly since morphological transformations can be used to monitor "physiological" responses at the same time within the same cell.


2021 ◽  
Vol 1 (5) ◽  
pp. 86-91
Author(s):  
O. B. Dronova ◽  
E. V. Kolesnikova ◽  
A. N. Neverov ◽  
S. V. Petrov ◽  
S. V. Miroshnikov

The article presents some information about xanthomatosis, as well as about xanthomas of the stomach, which are benign formations, but their etiopathogenesis is unknown. Some believe that there is a relationship between xanthomas of the stomach and hyperlipidymia, diabetes, preneoplastic changes in the mucous membrane, age-related features of the gastric mucosa.The clinical case described in this report confi rms the existing point of view about xanthomas as markers of preneopastic changes in the gastric mucosa and its precancerous diseases.


2002 ◽  
Vol 2 ◽  
pp. 1643-1645 ◽  
Author(s):  
John Graham

Acid-secreting parietal cells from the gastric mucosa are widely studied as a model in studies on ion transport and the endocrine/paracrine ECL cells effectively control parietal cell function. Discontinuous gradients of iodixanol for the purification of ECL cells were subsequently simplified to the use of a density barrier. This technique is now commonly used following initial centrifugal elutriation.


2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Satoshi Yamashita ◽  
Sohachi Nanjo ◽  
Emil Rehnberg ◽  
Naoko Iida ◽  
Hideyuki Takeshima ◽  
...  

Abstract Background Aberrant DNA methylation is induced by aging and chronic inflammation in normal tissues. The induction by inflammation is widely recognized as acceleration of age-related methylation. However, few studies addressed target genomic regions and the responsible factors in a genome-wide manner. Here, we analyzed methylation targets by aging and inflammation, taking advantage of the potent methylation induction in human gastric mucosa by Helicobacter pylori infection-triggered inflammation. Results DNA methylation microarray analysis of 482,421 CpG probes, grouped into 270,249 genomic blocks, revealed that high levels of methylation were induced in 44,461 (16.5%) genomic blocks by inflammation, even after correction of the influence of leukocyte infiltration. A total of 61.8% of the hypermethylation was acceleration of age-related methylation while 21.6% was specific to inflammation. Regions with H3K27me3 were frequently hypermethylated both by aging and inflammation. Basal methylation levels were essential for age-related hypermethylation while even regions with little basal methylation were hypermethylated by inflammation. When limited to promoter CpG islands, being a microRNA gene and high basal methylation levels strongly enhanced hypermethylation while H3K27me3 strongly enhanced inflammation-induced hypermethylation. Inflammation was capable of overriding active transcription. In young gastric mucosae, genes with high expression and frequent mutations in gastric cancers were more frequently methylated than in old ones. Conclusions Methylation by inflammation was not simple acceleration of age-related methylation. Targets of aberrant DNA methylation were different between young and old gastric mucosae, and driver genes were preferentially methylated in young gastric mucosa.


2000 ◽  
Vol 278 (6) ◽  
pp. G855-G865 ◽  
Author(s):  
Zhi-Qiang Xiao ◽  
Adhip P. N. Majumdar

Although aging enhances expression and tyrosine kinase activity of epidermal growth factor receptor (EGFR) in the gastric mucosa, there is no information about EGFR signaling cascades. We examined the age-related changes in mitogen-activated protein kinases (MAPKs) [extracellular signal-related kinases (ERKs), c-Jun NH2-terminal kinases (JNKs), and p38], an EGFR-induced signaling cascade, and activator protein-1 (AP-1) and nuclear factor-κB (NF-κB) transcriptional activity in the gastric mucosa of 4- to 6-, 12- to 14-, and 22- to 24-mo-old Fischer 344 rats. AP-1 and NF-κB transcriptional activity in the gastric mucosa rose steadily with advancing age. This can be further induced by transforming growth factor-α. The age-related activation of AP-1 and NF-κB in the gastric mucosa was associated with increased levels of c-Jun, c-Fos, and p52, but not p50 or p65. Total and phosphorylated IκBα levels in the gastric mucosa were unaffected by aging. Aging was also associated with marked activation of ERKs (p42/p44) and JNK1. In contrast, aging decreased p38 MAPK activity in the gastric mucosa. Our observation of increased activation of ERKs and JNK1 in the gastric mucosa of aged rats suggests a role for these MAPKs in regulating AP-1 and NF-κB transcriptional activity. These events may be responsible for the age-related rise in gastric mucosal proliferative activity.


1999 ◽  
Vol 277 (5) ◽  
pp. G929-G934 ◽  
Author(s):  
Zhi-Qiang Xiao ◽  
Yingjie Yu ◽  
Ahmed Khan ◽  
Richard Jaszewski ◽  
Murray N. Ehrinpreis ◽  
...  

Although in Fischer 344 rats aging is found to be associated with increased gastric mucosal proliferative activity, little is known about specific changes in the regulatory mechanisms of this process. To determine whether changes in cell cycling events could partly contribute to the age-related rise in gastric mucosal proliferative activity, the present investigation examines changes in cyclin-dependent kinase (Cdk2) activity and the regulation of this process in the gastric mucosa of Fischer 344 rats aged 4 (young), 13 (middle aged), and 24 (old) mo. We observed that aging is associated with a progressive rise in activity and protein levels of Cdk2 in the gastric mucosa. This is also found to be accompanied by a concomitant increase in cyclin E but not cyclin D1 levels. On the other hand, the levels of p21Waf1/Cip1 (total as well as the fraction associated with Cdk2), a nuclear protein that is known to inhibit different cyclin-Cdk complexes, are found to decline in the gastric mucosa with advancing age. In contrast, with aging, there was a steady rise in p53 levels in the gastric mucosa. We have also observed that the levels of phosphorylated retinoblastoma protein, a form that participates in regulating progression through the S phase, are markedly elevated in the gastric mucosa of aged rats. In conclusion, our data suggest that, in the gastric mucosa, aging enhances transition of G1 to S phase as well as progression through the S phase of the cell cycle. However, the age-related decline in p21Waf1/Cip1 in the gastric mucosa appears to be independent of p53 status.


PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e81473 ◽  
Author(s):  
Paolo Trevisi ◽  
Greta Gandolfi ◽  
Davide Priori ◽  
Stefano Messori ◽  
Michela Colombo ◽  
...  

2001 ◽  
Vol 280 (6) ◽  
pp. C1599-C1606 ◽  
Author(s):  
Ann M. Sherry ◽  
Danuta H. Malinowska ◽  
Randal E. Morris ◽  
Georgianne M. Ciraolo ◽  
John Cuppoletti

HCl secretion across the parietal cell apical secretory membrane involves the H+-K+-ATPase, the ClC-2 Cl− channel, and a K+ channel. In the present study, the cellular and subcellular distribution of ClC-2 mRNA and protein was determined in the rabbit gastric mucosa and in isolated gastric glands. ClC-2 mRNA was localized to parietal cells by in situ hybridization and by direct in situ RT-PCR. By immunoperoxidase microscopy, ClC-2 protein was concentrated in parietal cells. Immunofluorescent confocal microscopy suggested that the ClC-2 was localized to the secretory canalicular membrane of stimulated parietal cells and to intracellular structures of resting parietal cells. Immunogold electron microscopy confirmed that ClC-2 is in the secretory canalicular membrane of stimulated cells and in tubulovesicles of resting parietal cells. These findings, together with previous functional characterization of the native and recombinant channel, strongly indicate that ClC-2 is the Cl− channel, which together with the H+-K+-ATPase and a K+ channel, results in HCl secretion across the parietal cell secretory membrane.


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