Reproductive cells and peripheral parietal cells collaboratively participate in meiotic fate acquisition in rice anthers

2021 ◽  
Author(s):  
Tingting Zhao ◽  
Ren Lijun ◽  
Yangzi Zhao ◽  
Hanli You ◽  
Yue Zhou ◽  
...  
Keyword(s):  
Parietal Cells

La3+ and pH sensitivity of Ca2+ entry and intracellular store filling in gastric parietal cells

1995 ◽  
Vol 269 (5) ◽  
pp. G770-G778 ◽  
Author(s):  
P. A. Negulescu ◽  
T. E. Machen
Keyword(s):  
Positive Feedback ◽  
Low Ph ◽  
Parietal Cells ◽  
Additional Increase ◽  
Cholinergic Agonist ◽  
Intracellular Store ◽  
Entry Pathway ◽  
Signaling Function ◽  
Previously Treated ◽  
Gastric Parietal Cells

The fluorescent Ca2+ indicator fura 2 was used to measure cytosolic free [Ca2+] ([Ca2+]i) in order to obtain information about relative rates of Ca2+ influx into parietal cells during treatment with carbachol (a cholinergic agonist) or thapsigargin (TG, a Ca(2+)-mobilizing agent) or during reloading of the internal Ca2+ stores. In Ca(2+)-containing solutions, carbachol-, TG-, and reloading-stimulated Ca2+ entry exhibited nearly identical sensitivity to La3+ [inhibition constant (Ki) approximately 10 microM] or low pH (pKi approximately 7.0). In experiments in which carbachol and TG were used, there was no additional increase in [Ca2+]i when TG was added to carbachol-treated cells or when carbachol was added to cells previously treated with TG. Thus it is likely that a single Ca2+ entry pathway serves a signaling function as well as a role in refilling the Ca2+ store during reloading. Because the Ca2+ pathway is exquisitely sensitive to pH and serosal pH increases during stimulant-induced H+ secretion (which is activated by increases in [Ca2+]i), this mechanism will exert positive feedback on parietal cells in the intact stomach. When parietal cells were pretreated with carbachol in Ca(2+)-free solutions, reloading was independent of pH and La3+, suggesting that Ca(2+)-containing solutions should be used to determine the properties of the influx pathway.

scholarly journals Regulation of free cytosolic Ca2+ in the peptic and parietal cells of the rabbit gastric gland.

1986 ◽  
Vol 261 (6) ◽  
pp. 2660-2667
Author(s):  
S Muallem ◽  
C J Fimmel ◽  
S J Pandol ◽  
G Sachs
Keyword(s):  
Gastric Gland ◽  
Parietal Cells

scholarly journals Receptor-operated Ca2+ channels in gastric parietal cells: gastrin and carbachol induce Ca2+ influx in depleting intracellular Ca2+ stores

1993 ◽  
Vol 289 (1) ◽  
pp. 117-124 ◽  
Author(s):  
S Roche ◽  
J P Bali ◽  
R Magous
Keyword(s):  
Steady State ◽  
Receptor Activation ◽  
Parietal Cells ◽  
The Other ◽  
Bivalent Cation ◽  
Gtp Binding ◽  
Gastric Parietal Cells ◽  
Type Receptor ◽  
Ca2 Channels ◽  
Stimulation Of

The mechanism whereby gastrin-type receptor and muscarinic M3-type receptor regulate free intracellular Ca2+ concentration ([Ca2+]i) was studied in rabbit gastric parietal cells stimulated by either gastrin or carbachol. Both agonists induced a biphasic [Ca2+]i response: a transient [Ca2+]i rise, followed by a sustained steady state depending on extracellular Ca2+. Gastrin and carbachol also caused a rapid and transient increase in Mn2+ influx (a tracer for bivalent-cation entry). Pre-stimulation of cells with one agonist drastically decreased both [Ca2+]i increase and Mn2+ influx induced by the other. Neither diltiazem nor pertussistoxin treatment had any effect on agonist-stimulated Mn2+ entry. Thapsigargin, a Ca(2+)-pump inhibitor, induced a biphasic [Ca2+]i increase, and enhanced the rate of Mn2+ entry. Preincubation of cells with thapsigargin inhibits the [Ca2+]i increase as well as Mn2+ entry stimulated by gastrin or by carbachol. Thapsigargin induced a weak but significant increase in Ins(1,4,5)P3 content, but this agent had no effect on the agonist-evoked Ins(1,4,5)P3 response. In permeabilized parietal cells, Ins(1,4,5)P3 and caffeine caused an immediate Ca2+ release from intracellular pools, followed by a reloading of Ca2+ pools which can be prevented in the presence of thapsigargin. We conclude that (i) gastrin and carbachol mobilize common Ca2+ intracellular stores, (ii) Ca2+ permeability secondary to receptor activation involves neither a voltage-sensitive Ca2+ channel nor a GTP-binding protein from the G1 family, and (iii) agonists regulate common Ca2+ channels in depleting intracellular Ca2+ stores.

Succinic and Malic Oxidase in Gastric Hydrochloric Acid Production

1956 ◽  
Vol 187 (3) ◽  
pp. 427-431 ◽  
Author(s):  
Joseph J. Vitale ◽  
Oscar M. Jankelson ◽  
Patricia Connors ◽  
D. Mark Hegsted ◽  
Norman Zamcheck
Keyword(s):  
Gastric Mucosa ◽  
Guinea Pig ◽  
Succinic Dehydrogenase ◽  
Titratable Acidity ◽  
Spectrophotometric Analysis ◽  
Parietal Cells ◽  
Human Gastric Mucosa ◽  
City Hospital ◽  
Malic Dehydrogenase ◽  
Oxidase System

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.

Ink4a/Arf-Dependent Loss of Parietal Cells Induced by Oxidative Stress Promotes CD44-Dependent Gastric Tumorigenesis

2015 ◽  
Vol 8 (6) ◽  
pp. 492-501 ◽  
Author(s):  
Ryo Seishima ◽  
Takeyuki Wada ◽  
Kenji Tsuchihashi ◽  
Shogo Okazaki ◽  
Momoko Yoshikawa ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parietal Cells

Secretion of gastric parietal cells

1958 ◽  
Vol 14 (6) ◽  
pp. 204-205 ◽  
Author(s):  
D. Birnbaum ◽  
M. Wolman
Keyword(s):  
Parietal Cells ◽  
Gastric Parietal Cells

The effects of rabeprazole on ECL cells and parietal cells in rat -comparison with omeprazole

2000 ◽  
Vol 118 (4) ◽  
pp. A1110
Author(s):  
Akira Tari ◽  
Masanori Kawano ◽  
Toyohiko Aoki ◽  
Yoshikazu Yonei ◽  
Kanji Kodama ◽  
...  
Keyword(s):  
Parietal Cells ◽  
Ecl Cells

Demonstration of gap junctional protein connexin 32 and connexin 26 among parietal cells of mammalian gastric glands

1998 ◽  
Vol 114 ◽  
pp. A1171
Author(s):  
Gilbert R. Ortega ◽  
Rosh Caroppo ◽  
Edgar B. Rodas ◽  
Athar M. Qureshi ◽  
David C. Spray ◽  
...  
Keyword(s):  
Parietal Cells ◽  
Connexin 26 ◽  
Connexin 32 ◽  
Gastric Glands ◽  
Junctional Protein ◽  
Gap Junctional
Sign in / Sign up

Export Citation Format

Share Document