Anion secretion induced by capacitative Ca2+ entry through apical and basolateral membranes of cultured equine sweat gland epithelium.
Abstract: 1. Anion secretion induced by capacitative Ca2+ entry through apical and basolateral membranes of cultured equine sweat gland epithelium was studied using the short-circuit current (Isc) technique. 2. Thapsigargin induced an increase in Isc that could be inhibited when external Ca2+ was chelated by EGTA. 3. The inhibition of the thapsigargin-induced Isc could be reversed by re-addition of Ca2+ to apical or basolateral solutions. The magnitude of the reactivated Isc depended predominantly on basolateral Ca2+ concentration. 4. The magnitude of the reactivated Isc upon basolateral Ca2+ addition increased with the thapsigargin concentration, indicating its dependence on the emptied state of the Ca2+ store induced by thapsigargin. 5. The thapsigargin-induced Isc, as well as the Ca(2+)-dependent reactivation of Isc in EGTA-treated epithelia, was inhibitable by apical, but not basolateral, addition of flufenamate, and by basolateral addition of La3+. Other Ca2+ channel blockers, verapamil and nifedipine, had no effect when applied to either membrane. 6. The results suggest that thapsigargin-induced anion secretion by the equine sweat gland epithelial cells is crucially dependent upon the Ca2+ influx occurring primarily through the basolateral membrane, and that apical and basolateral membranes may possess different pathways for Ca2+ entry.
Publication Date: 1996-11-15 PubMed ID: 8951708PubMed Central: PMC1160909DOI: 10.1113/jphysiol.1996.sp021746Google Scholar: Lookup
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- Journal Article
- Research Support
- Non-U.S. Gov't
Summary
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This research investigates how the entry of calcium molecules into cells of horse sweat glands influences anion secretion, which contributes to sweating. The study uses a technique known as short-circuit current to evaluate this process, and further examines how it is affected by various inhibitors and concentrations.
Methodology and Key Findings
- The research utilized a methodology known as the short-circuit current (Isc) technique. This approach allowed the researchers to study anion secretion – the process by which negatively charged ions are released – in the cultured cells of equine (horse) sweat glands.
- Thapsigargin, a substance known to impact calcium levels in cells, led to an increase in the Isc. This increase could be prevented by using a chemical called EGTA to bind with and remove calcium atoms from the outer cell environment.
- Interestingly, the inhibition of the thapsigargin-induced increase in Isc could be reversed. This was achieved by reintroducing calcium to the apical membrane (the surface of the cell that faces towards the inner body) or the basolateral membrane (the surface of the cell facing away from the body’s interior). The extent of this reversal relied mainly on the concentration of calcium atoms at the basolateral membrane.
- Finding that the extent of Isc reactivation increased with higher concentrations of thapsigargin suggests that this recovery process depends on how depleted the cell’s internal calcium store is – a state that is triggered by thapsigargin.
Role of Apical and Basolateral Membranes
- This increase in Isc, as well as the calcium-dependent reactivation of Isc in cells treated with EGTA, could be blocked by introducing flufenamate to the apical membrane, or La3+ to the basolateral membrane. Other substances known to block calcium channels, like verapamil and nifedipine, had no observable effects when applied to either membrane.
- This suggests that the process by which thapsigargin promotes anion secretion in equine sweat gland cells relies significantly on the influx of calcium, and that it is primarily taking place at the basolateral membrane. Furthermore, the differing effects of these substances imply that the apical and basolateral membranes may have different pathways for calcium entry into the cell.
Cite This Article
APA
Ko WH, Chan HC, Wong PY.
(1996).
Anion secretion induced by capacitative Ca2+ entry through apical and basolateral membranes of cultured equine sweat gland epithelium.
J Physiol, 497 ( Pt 1)(Pt 1), 19-29.
https://doi.org/10.1113/jphysiol.1996.sp021746 Publication
Researcher Affiliations
- Department of Physiology, Faculty of Medicine, Chinese University of Hong Kong, Shatin, NT, Hong Kong. whko@cuhk.edu.hk
MeSH Terms
- Animals
- Anions / metabolism
- Calcimycin / pharmacology
- Calcium / metabolism
- Calcium / pharmacology
- Cell Membrane / metabolism
- Cells, Cultured
- Chelating Agents / pharmacology
- Egtazic Acid / pharmacology
- Electrophysiology
- Flufenamic Acid / pharmacology
- Horses
- Ionophores / pharmacology
- Lanthanum / pharmacology
- Sweat Glands / metabolism
- Thapsigargin / pharmacology
References
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Citations
This article has been cited 5 times.- Shaw PJ, Feske S. Physiological and pathophysiological functions of SOCE in the immune system. Front Biosci (Elite Ed) 2012 Jan 1;4(6):2253-68.
- Berna-Erro A, Woodard GE, Rosado JA. Orais and STIMs: physiological mechanisms and disease. J Cell Mol Med 2012 Mar;16(3):407-24.
- Feske S. CRAC channelopathies. Pflugers Arch 2010 Jul;460(2):417-35.
- Feske S. ORAI1 and STIM1 deficiency in human and mice: roles of store-operated Ca2+ entry in the immune system and beyond. Immunol Rev 2009 Sep;231(1):189-209.
- Kim SJ, Nam JH, Woo JE, Kim SJ, Rhee PL. Ca(2+) influx through the basolateral- and luminal membranes of colonic epithelium in neonatal rats. Pflugers Arch 2004 Jan;447(4):408-15.
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