scholarly journals Electrical coupling and uncoupling of exocrine acinar cells.

1978 ◽  
Vol 79 (2) ◽  
pp. 533-545 ◽  
Author(s):  
N Iwatsuki ◽  
O H Petersen
Keyword(s):  
Electrical Coupling ◽  
Acinar Cells ◽  
Potential Change ◽  
Coupling Coefficients ◽  
Cell Coupling ◽  
Pancreatic Cell ◽  
Membrane Area ◽  
Acinar Tissue ◽  
Lacrimal Acinar Cells ◽  
Electrotonic Potential

The electrical communication network in the mouse pancreatic acinar tissue has been investigated using simultaneous intracellular recording with two separate microelectrodes and direct microscopical control of the localizations of the microelectrode tips. All cells within one acinus were electrically coupled, and the coupling coefficient (the electrotonic potential change in a cell neighboring to the cell into which current is injected [V2] divided by the electrotonic potential change in the cell of current injection [V1]) between two cells near each other (less than 50 micron) was always close to 1. Cells farther apart (50-100 micron) were, in some cases, coupled; in other cases, there was no coupling at all. Coupling coefficients varied between 0 and 1. There was rarely electrical coupling over distances of more than 110 micron. Using microiontophoretic acetylcholine (ACh) application, it was possible to evoke almost complete electrical uncoupling of two previously coupled pancreatic or lacrimal acinar cells from different acini or within one acinus. The effects were fully and quickly reversible. While the ACh-evoked uncoupling in the pancreas was associated with membrane depolarization, ACh caused hyperpolarization in the lacrimal acinar cells. The uncoupling was associated with a very marked reduction in electrical time constant, indicating a reduction in input capacitance (effective surface cell membrane area). The concentrations of stimulants needed to evoke reduction in pancreatic cell-to-cell coupling were 1 micron for ACh, 0.14 nM for caerulein, and 3 nM for bombesin. These concentrations are smaller than those required to evoke maximal enzyme secretion.

Ultrastructure of isolated and cultured rat pancreatic ducts

1978 ◽  
Vol 36 (2) ◽  
pp. 530-531
Author(s):  
J. R. Ruby ◽  
S. Githens ◽  
D. R. G. Holmquist
Keyword(s):  
Acinar Cells ◽  
Duct Cell ◽  
Epithelial Tissue ◽  
Pancreatic Ducts ◽  
Cell Type ◽  
Pancreatic Cell ◽  
Duct Epithelium ◽  
Ficoll Gradient ◽  
Before And After ◽  
Acinar Tissue

Carcinoma of the exocrine pancreas in humans will often appear morphologically like duct epithelial tissue. It is not known, however, if such duct cell adenocarcinoma arise from duct cells directly, or from the neoplastic transformation of another pancreatic cell type such as the acinar cells. In either case, a better understanding of this type of cancer is necessary. To date, most of the information concerning pancreatic duct epithelium has been based primarily on studies of the intact pancreas. Thus, this investigation was an attempt to isolate rat pancreatic ducts so that they could be studied ultrastructurally and biochemically before and after culture. The ultimate intent is to expose the cultured ducts to carcinogens, in order to determine which carcinogens have an effect on duct tissue, and the nature of such effects.Juvenile rat pancreases were digested with collagenase and duct fragments were separated from acinar tissue by flotation through a Ficoll gradient or by filtration through stainless steel sieves.

Effects of MeCh, thapsigargin, and La3+ on plasmalemmal and intracellular Ca2+ transport in lacrimal acinar cells

1990 ◽  
Vol 258 (6) ◽  
pp. C1006-C1015 ◽  
Author(s):  
C. Y. Kwan ◽  
H. Takemura ◽  
J. F. Obie ◽  
O. Thastrup ◽  
J. W. Putney
Keyword(s):  
Plasma Membrane ◽  
Muscarinic Receptor ◽  
Extracellular Space ◽  
Receptor Agonist ◽  
Inositol Phosphates ◽  
Acinar Cells ◽  
Direct Channel ◽  
Physiological Conditions ◽  
Parotid Cells ◽  
Lacrimal Acinar Cells

The Ca2(+)-mobilizing actions of the muscarinic receptor agonist, methacholine (MeCh), and the microsomal Ca2+ pump inhibitor, thapsigargin, were investigated in lacrimal acinar cells. As previously shown for parotid cells (J. Biol. Chem. 264: 12266-12271, 1989), thapsigargin activates both internal Ca2+ release and Ca2+ entry from the extracellular space without increasing cellular inositol phosphates. The inorganic Ca2+ antagonist La3+ inhibited MeCh- or thapsigargin-activated Ca2+ entry. However, when added before MeCh or thapsigargin, La3+ inhibited the extrusion of Ca2+ at the plasma membrane. This phenomenon was exploited in protocols designed to investigate the pathways for filling agonist-sensitive Ca2+ stores in lacrimal cells. The results show that, in contrast to previous suggestions that external Ca2+ is required to replenish agonist-regulated Ca2+ stores, the inhibition of Ca2+ extrusion permits recycling of Ca2+ released by MeCh back into an MeCh- and thapsigargin-sensitive pool. Thus, although extracellular Ca2+ is the major source for refilling the intracellular Ca2+ stores under physiological conditions, the pathway by which this Ca2+ enters the pool need not be a direct one. These results are consistent with the recently revised capacitative model for the refilling of intracellular Ca2+ stores through Ca2+ influx subsequent to Ca2+ depletion, according to which refilling of intracellular Ca2+ stores occurs via a cytoplasmic route rather than a direct channel between intracellular Ca2+ stores and the extracellular space.

Discovering the mechanism of capacitative calcium entry

2006 ◽  
Vol 291 (6) ◽  
pp. C1104-C1106 ◽  
Author(s):  
Juan A. Rosado
Keyword(s):  
Acinar Cells ◽  
Calcium Entry ◽  
Capacitative Calcium Entry ◽  
Historical Significance ◽  
Intracellular Ca ◽  
Lacrimal Acinar Cells ◽  
Classic Paper

This essay examines the historical significance of an APS classic paper that is freely available online: Kwan CY, Takemura H, Obie JF, Thastrup O, and Putney JW Jr. Effects of MeCh, thapsigargin, and La3+ on plasmalemmal and intracellular Ca2+ transport in lacrimal acinar cells. Am J Physiol Cell Physiol 258: C1006–C1015, 1990. ( http://ajpcell.physiology.org/cgi/reprint/258/6/C1006 )

scholarly journals Induction of pancreatic acinar cell proliferation by thyroid hormone

2005 ◽  
Vol 185 (3) ◽  
pp. 393-399 ◽  
Author(s):  
G M Ledda-Columbano ◽  
A Perra ◽  
M Pibiri ◽  
F Molotzu ◽  
A Columbano
Keyword(s):  
Cell Proliferation ◽  
Thyroid Hormone ◽  
Dna Synthesis ◽  
Acinar Cell ◽  
Acinar Cells ◽  
Pancreatic Acinar Cell ◽  
Labeling Index ◽  
Metabolic Effects ◽  
Brdu Incorporation ◽  
Pancreatic Cell

Thyroid hormone is known to elicit diverse cellular and metabolic effects in various organs, including mitogenesis in the rat liver. In the present study, experiments were carried out to determine whether thyroid hormone is able to stimulate cell proliferation in another quiescent organ such as the pancreas. 3,5,3′-l-tri-iodothyronine (T3) added to the diet at a concentration of 4 mg/kg caused a striking increase in nuclear bromodeoxyuridine (BrdU) incorporation of rat acinar cells 7 days after treatment (the labeling index was 46.7% in T3-treated rats vs 7.1% in controls). BrdU incorporation was limited to the acinar cells, with duct cells and islet cells being essentially negative. The increase in DNA synthesis was accompanied by the presence of several mitotic figures. Histological examination of the pancreas did not exhibit any sign of T3-induced toxicity. Determination of the apoptotic index, measurement of the serum levels of α-amylase and lipase, and glycemia determination did not show any increase over control values, suggesting that the enhanced proliferation of acinar cells was a direct effect induced by T3 and not a regenerative response consequent to acinar or β-cell injury. Additional experiments showed that DNA synthesis was induced as early as 2 days after T3 treatment (the labeling index was 9.4 vs 1.9% in controls) and was associated with increased protein levels of cyclin D1, cyclin A and proliferating cell nuclear antigen, with no substantial differences in the expression of the cyclin-dependent kinase inhibitor p27. The mitogenic effect of T3 on the pancreas was not limited to the rat, since extensive acinar cell proliferation was also observed in the pancreas of mice treated with T3 for 1 week (the labeling index was 28% in T3-treated mice vs 1.8% in controls). Treatment with three other ligands of nuclear receptors, ciprofibrate, all-trans retinoic acid and 1,4-bis[2-(3,5-dichloropyridyloxy)]benzene, induced little or no pancreatic cell proliferation. These results demonstrated that T3 is a powerful inducer of cell proliferation in the pancreas and suggested that pancreatic acinar cell proliferation by selected agents may have potential for therapeutic use.

IL-2 Immunoreactive Proteins in Lacrimal Acinar Cells

2002 ◽  
pp. 795-799 ◽  
Author(s):  
Yan Zhang ◽  
Jiansong Xie ◽  
Limin Qian ◽  
Joel E. Schechter ◽  
Austin K. Mircheff
Keyword(s):  
Acinar Cells ◽  
Lacrimal Acinar Cells
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