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4 edition of Regulation of Ca2+ influx in salivary acinar cells found in the catalog.

Regulation of Ca2+ influx in salivary acinar cells

Neela D. Rampersad

Regulation of Ca2+ influx in salivary acinar cells

by Neela D. Rampersad

  • 278 Want to read
  • 23 Currently reading

Published by National Library of Canada in Ottawa .
Written in English


Edition Notes

SeriesCanadian theses = -- Thèses canadiennes
The Physical Object
FormatMicroform
Pagination2 microfiches : negative. --
ID Numbers
Open LibraryOL17042290M
ISBN 100315963301
OCLC/WorldCa222159009

  The fusion process itself is Ca2+-dependent. However, earlier stages of the process, e.g. ‘docking’ could be cAMP-dependent. In salivary gland cells, this step is the rate- limiting ‘brake’ point in exocytosis. Polymeric IgA and IgM are transported across salivary gland cells by the polymeric immunoglobulin receptor (pIgR).   Salivary gland acinar hypertrophy should be diagnosed and graded based on the degree of increase in acinar cell size and number of cells affected. Multifocal hypertrophy would be assigned a higher severity grade than focal hypertrophy. If the hypertrophy is diffuse throughout the gland, then the modifier "diffuse" should be added to the diagnosis.

Therefore, the passive Na and Cl influx and the cytoplasmic Ca flowed in from extracellular spaces and released from secretory granules, an intracellular calcium store, by secretory stimulation probably triggers the passive or active Na and CL extrusion and consequently the osmotic water flux from the basal part of acinar cells to the secretory. Aure MH, Røed A, Kanli Galtung H. Intracellular Ca 2+ responses and cell volume regulation upon cholinergic and purinergic stimulation in an immortalized salivary cell line. Eur J Oral Sci ;

Salivary Glands and Saliva. Saliva is produced in and secreted from salivary glands. The basic secretory units of salivary glands are clusters of cells called an acini. These cells secrete a fluid that contains water, electrolytes, mucus and enzymes, all of which flow out of the acinus into collecting ducts. Ca2+ is an integral mediator of intracellular signaling, impacting almost every aspect of cellular life. The Ca2+-conducting transporters located on the endoplasmic reticulum (ER) membrane shoulder the responsibility of constructing the global Ca2+ signaling landscape. These transporters gate the ER Ca2+ release and uptake, sculpt signaling duration and intensity, and compose the Ca2.


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Regulation of Ca2+ influx in salivary acinar cells by Neela D. Rampersad Download PDF EPUB FB2

Ca 2+ influx has been long recognized as the primary factor regulating sustained fluid secretion from salivary acinar cells (1,2,7,8,14). Earlier studies established that Ca 2+ influx into cells is increased several fold following stimulation of the cells with an agonist suggesting that it is dependent on receptor activation (1, 10).Cited by:   1.

Introduction. Neurotransmitter-generated Ca 2+ signals in exocrine gland cells, such as pancreatic and salivary gland acinar cells, are critical for the regulation of their secretory functions; fluid secretion in salivary acinar cells and protein secretion in pancreatic acinar cells.Under normal physiological conditions, salivary glands maintain a continuous low level of saliva Cited by: Neurotransmitter-regulation of fluid secretion in the salivary glands is achieved by a coordinated sequence of intracellular signaling events, including the activation of membrane receptors, generation of the intracellular second messenger, inositol 1,4,5, trisphosphate, internal Ca 2+ release, and Ca 2+ influx.

The resulting increase in cytosolic [Ca 2+] ([Ca 2+] i) regulates a number of ion Cited by: Most critical in this is the regulation of cytosolic free [Ca2+] ([Ca2+]i) in response to neurotransmitter stimulation.

Control of [Ca2+]i increase in specific regions of the cell is the main determinant of fluid and electrolyte secretion in salivary gland acinar cells as it regulates several major ion flux mechanisms as well as the water Cited by: Summary. Measurement and manipulation of cytoplasmic free Ca 2+ in intact pancreatic acinar cells have suggested its primary role in regulating secretion in response to acetylcholine and cholecystokinin.

Evidence suggests that Ca 2+ is initially released from an intracellular store but increased Ca 2+ entry is required for maintained stimulation. The mechanism of increased Ca 2+ entry is Cited by: 3. In general, in nonexcitable cells this elevation of [Ca2+]i results from two sources: an initial release of Ca2+ from intracellular stores followed by an influx of extracellular Ca2+.

These two phases, release from intracellular stores and Ca2+ influx, are generally coupled: stimulation of influx is coordinated with depletion of Ca2+ from.

Tyrosine kinase inhibitors attenuate "capacitative" Ca2+ influx in rat pancreatic acinar cells. Biochem Biophys Res Commun (3):PMID: Yule DI, Lawrie AM and Gallacher DV.

Acetylcholine and cholecystokinin induce different patterns of oscillating calcium signals in pancreatic acinar cells. Cell Calcium 12(): Taken up by the Ca2+ Stores in the Rat Salivary Acinar Cells.

Tohoku J. Exp. Med.,(2), When Sr2+ was introduced to the external solution after the depletion of Ca2+ from stores of submandibular acinar cells by ACh. Agonist-induced Ca2+ entry via store-operated Ca2+ (SOC) channels is suggested to regulate a wide variety of cellular functions, including salivary gland fluid secretion.

However, the molecular components of these channels and their physiological function(s) are largely unknown. Here we report that attenuation of SOC current underlies salivary gland dysfunction in mice lacking. Regulation ofCa2+Influx in MyeloidCells Roleof PlasmaMembranePotential, Inositol Phosphates,Cytosolic Free[Ca2+J, andFilling Stateof IntracellularCa2+Stores NicolasDemaurex,* WernerSchlegel,t PeterVarnai,' GeorgMayr,11 Daniel P.

Lew,* andKarl-Heinz Krause* *Infectious DiseasesDivision, UniversityHospitalGeneva, CH Geneva4, Switzerland;tFondationpour.

We conclude that Ca2+ regulation in SMG-C6 cells is similar to that in freshly isolated SMG acinar cells; therefore, this cell line represents an excellent SMG cell model in terms of intracellular.

the cells in the end piece are arranged in a roughly spherical form. In mucous glands they tend to be arranged in a tubular configuration with a larger central lumen.

In both types of gland the cells in the end piece surround a lumen and this is the start of the ductal system. There are three types of duct present in all salivary glands. The. elevated [Ca2+]i duringreceptor stimulation.

Inthepresent studywehaveexaminedthe role ofNa+in theregulation ofboth pHiand[Ca2+]i in rabbitmandibularglandacinar cells. Previousworkbyourselves and others (Lau et al. ; Steward et al. ) has suggested the presence of Na+-H+exchange in rabbit mandibular acinar cells.

In the present workwe have. This situation leads to the lack of reports on the in vitro cell biology and physiology of human salivary gland cells.

This study used a low‐calcium culture system to selectively cultivate human parotid gland acinar (PGAC) cells from tissues with high purity in cell composition. Peter Thorn's 82 research works with 2, citations and 3, reads, including: A fluorescent timer reporter enables sorting of insulin secretory granules by age.

To study changes in the cytoplasmic Ca2+ concentration ([Ca2+]i) and the total amount of calcium in cells, we used, respectively, the fluorescent dye fura 2/AM and the metallochrome dye arsenazo III.

The total amount of calcium in acinar cells after their incubation in calcium-free ATP-containing extracellular solution decreased. The action of ATP induced a dose-dependent increase in the [Ca2. The work of Aure et al. supports a model for salivary gland homeostasis based predominantly on self-duplication of secretory cells, rather than on differentiation of stem cells.

The proliferative capacity of differentiated secretory cells may prove critical in the implementation of cell-based strategies to restore damaged salivary glands after radiation.

Ca2+ Responses and Spontaneous Ca2+ Oscillations [Ca2+]i elevations in salivary acinar and ductal cells induce cell shrinkage. These changes in cell vol­ume are thought to reflect changes in the solute con­ A.

Tanimura, et al:Calcium Responses in Salivary Ducts Fig. 3 Changes in the shape of parotid duct cells(A)CCh-induced enlargement of the.

In salivary acinar cells, the pattern of the Ca2+ signals that regulates fluid and enzyme secretion has yet to be resolved, as there are conflicting reports in the literature. We have used a two-photon technique to directly visualize the acinar cell lumen in living fragments of exocrine tissue and simultaneously recorded agonist-induced changes in intracellular Ca2+.

at least some of the neoplastic cells demonstrate serous acinar cell differentiation characterized by cytoplasmic zymogen secretory granules. Salivary ductal cells can also be a component of this low-grade neoplasm that most often occurs in the parotid gland and presents at a relatively younger age than other salivary gland tumors.

Developmental Cell Short Article Salivary Gland Homeostasis Is Maintained through Acinar Cell Self-Duplication Marit H. Aure,1 Stephen F. Konieczny,2 and Catherine E.

Ovitt1,* 1Center for Oral Biology, Department of Biomedical Genetics, University of Rochester School of Medicine and Dentistry, Rochester, NYUSA 2Department of Biological Sciences, Purdue Center for Cancer Research.Pancreatitis is characterized by increased influx of Ca2+ into acinar cells, by unknown mechanisms.

Inhibitors of Ca2+ influx channels could be effective in treating acute pancreatitis, but these have deleterious side effects that can result in death. We investigated the expression patterns and functions of acinar cell Ca2+ channels and factors that regulate them during development of acute.HEK cells stably transfected with Gαqi and CCR2 genes were plated overnight in μl culture medium on a 96 well Biocoat poly-D lysine coated plate.

The next day, the cells were dye-loaded by adding μl 1X Dye-loading solution (BDTM Calcium Assay Kit) and incubating for 1 hour at 37˚C. MCP-1 was added (50 μl/well) by.