Mechanism for Carbachol-Induced Secretion of Lacritin in Cultured Monkey Lacrimal Acinar Cells

2010 ◽  
Vol 51 (9) ◽  
pp. 4395 ◽  
Author(s):  
Ayumi Morimoto-Tochigi ◽  
Ryan D. Walkup ◽  
Emi Nakajima ◽  
Thomas R. Shearer ◽  
Mitsuyoshi Azuma
Keyword(s):  
Acinar Cells ◽  
Lacrimal Acinar Cells

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 )

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

Potential Role of Disrupted Lacrimal Acinar Cells in Dry Eye during Pregnancy

2002 ◽  
pp. 153-157 ◽  
Author(s):  
Joel E. Schechter ◽  
Michael Pidgeon ◽  
Donald Chang ◽  
Yi-Ching Fong ◽  
Melvin D. Trousdale ◽  
...  
Keyword(s):  
Dry Eye ◽  
Potential Role ◽  
Acinar Cells ◽  
Lacrimal Acinar Cells

"BM180": a novel basement membrane protein with a role in stimulus-secretion coupling by lacrimal acinar cells

1996 ◽  
Vol 270 (6) ◽  
pp. C1743-C1750 ◽  
Author(s):  
G. W. Laurie ◽  
J. D. Glass ◽  
R. A. Ogle ◽  
C. M. Stone ◽  
J. R. Sluss ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Membrane Protein ◽  
Acinar Cells ◽  
Basement Membranes ◽  
Enzyme Linked Immunosorbent Assay ◽  
Regulated Secretion ◽  
Basement Membrane Protein ◽  
Stimulus Secretion Coupling ◽  
Lacrimal Acinar Cells ◽  
Laminin 1

Regulated secretion requires the developmental coupling of neuronal or hormonal stimuli to an exocytotic response, a multistep pathway whose appearance may be linked with cellular adhesion to the newly formed exocrine cell basement membrane. We screened for adhesion-associated coupling activity using lacrimal acinar cells and have identified “BM180”, a novel basement membrane protein enriched in guanidine HCl extracts of lacrimal and parotid exocrine secretory glands. BM180 resides primarily in a previously inexamined lower molecular-mass basement membrane peak (peak 2) that contains cell adhesion activity inhibitable with the anti-BM180 monoclonal antibody 3E12. Removal of peak 2 by gel filtration or preincubation of basement membrane with 3E12 decreased regulated peroxidase secretion by one-half without affecting constitutive secretion or the amount of cellular peroxidase available for release. Adding back peak 2 restored regulated secretion in a dose-dependent and 3E12-inhibitable manner and suggested a synergistic relationship between BM180 and laminin 1. BM180 has a mobility of 180 and 60 kDa in the absence or presence of dithiothreitol, respectively, and shows no immunological identity by competitive enzyme-linked immunosorbent assay with laminin 1, collagen IV, entactin, fibronectin, BM-40, perlecan, or vitronectin. We propose that BM180 is an important resident of certain glandular basement membranes where it interacts with the cell surface, thereby possibly signaling the appearance of a transducing element in the stimulus-secretion coupling pathway.

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