The Role of Calcium in the Volume Regulation of Rat Lacrimal Acinar Cells

1998 ◽  
Vol 164 (3) ◽  
pp. 283-291 ◽  
Author(s):  
T. Speake ◽  
I.J. Douglas ◽  
P.D. Brown
Keyword(s):  
Volume Regulation ◽  
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

POTENTIAL ROLE OF DISRUPTED LACRIMAL ACINAR CELLS IN DRY EYE DURING PREGNANCY.

Cornea ◽  
2000 ◽  
Vol 19 (Supplement 2) ◽  
pp. S121 ◽  
Author(s):  
Joel Schechter ◽  
Michael Pidgeon ◽  
Donald Chang ◽  
Yi-Ching Fong ◽  
Melvin Trousdale ◽  
...  
Keyword(s):  
Dry Eye ◽  
Potential Role ◽  
Acinar Cells ◽  
Lacrimal Acinar Cells

The Role of Gap Junctions in Lacrimal Acinar Cells: The Formation of Tears

2002 ◽  
pp. 109-113 ◽  
Author(s):  
Peter R. Brink ◽  
Virginijus Valiunas ◽  
Leon Moore ◽  
Aija Birzgalis ◽  
Benjamin Walcott
Keyword(s):  
Gap Junctions ◽  
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 )

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