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Store-mediated calcium entry in pleural mesothelial cells.
Masayoshi Kuwahara1, Maki Kuwahara
1Department of Comparative Pathophysiology, Graduate School of Agricultural and Life Sciences, The University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan. akuwam@mail.ecc.u-tokyo.ac.jp
European Journal of Pharmacology
|July 11, 2006
Summary
The actin cytoskeleton
Area of Science:
- Cell Biology
- Physiology
- Biochemistry
Background:
- Store-mediated calcium (Ca2+) entry is crucial for Ca2+ influx in non-excitable cells.
- The involvement of the actin cytoskeleton in this process remains controversial.
- Pleural mesothelial cells serve as a model to investigate this cellular mechanism.
Purpose of the Study:
- To investigate the role of the actin cytoskeleton in store-mediated Ca2+ entry in pleural mesothelial cells.
- To determine how cytoskeletal modifiers affect Ca2+ influx.
- To elucidate the mechanism underlying store-mediated Ca2+ entry in these cells.
Main Methods:
- Treatment of pleural mesothelial cells with thapsigargin to induce store-mediated Ca2+ entry.
- Application of cytoskeletal modifiers like mycalolide B and jasplakinolide.
- Assessment of intracellular Ca2+ levels ([Ca2+]i) using Ca2+ imaging.
- Pharmacological inhibition using nifedipine and SKF96365.
Main Results:
- Thapsigargin triggered store-mediated Ca2+ entry, confirmed by Ca2+ re-addition.
- Mycalolide B, which disrupts actin, did not inhibit Ca2+ entry.
- Jasplakinolide, however, prevented thapsigargin-induced Ca2+ entry, indicating a role for intact actin.
- SKF96365 blocked Ca2+ entry, while nifedipine did not.
Conclusions:
- The actin cytoskeleton plays a regulatory role in store-mediated Ca2+ entry in pleural mesothelial cells.
- Results support a secretion-like coupling model for store-mediated Ca2+ entry.
- Further research is needed to fully understand the dynamic interaction between actin and Ca2+ channels.