MLCK reciprocally regulates capacitative calcium entry and non-capacitative calcium entry in intracellular calcium influx process in mouse parotid gland acinar cells

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  • SAINO Tomoyuki
    Department of Anatomy （Cell Biology）, School of Dentistry, Iwate Medical University
  • KUMAGAI Miho
    Division of Special Care Dentistry, Department of Developmental Oral Health Science, School of Dentistry, Iwate Medical University
  • SATOH Yoh-ichi
    Department of Anatomy （Cell Biology）, School of Dentistry, Iwate Medical University Department of Medical Education, Iwate Medical University

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  • マウス耳下腺細胞でミオシン軽鎖キナーゼは細胞内カルシウム流入過程のcapacitative calcium entry, non-capacitative calcium entry を相反する形で制御する

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Abstract

<p>Arachidonic acid (AA) regulates intracellular calcium concentration in a variety of cell types. In the present study, the effects of serine/threonine phosphatases and myosin light chain kinase (MLCK) on AA-induced Ca2+ signaling in mouse parotid acinar cells were investigated.</p><p>Treatment of acinar cells with MLCK inhibitors, ML9 and wortmannin, thapsigargin-induced Ca2+ entry (capacitative Ca2+ entry: CCE) was partially blocked. In contrast, AA-induced Ca2+ entry (noncapacitative Ca2+ entry: NCCE) was attenuated by wortmannin but increased by ML9. Calyculin A, a protein phosphatase (PP) inhibitor, resulted in an enhancement of AA-induced Ca2+ entry. Our previous study suggested that this inhibition of PP resulted in an enhancement of AA-induced Ca2+ entry via PKA. In the presence of ML9, AA-induced Ca2+ influx enhanced by calyculin A was further increased. However, even when the order of ML9 administration was changed, the enhancement of AA-induced Ca2+ entry by calyculin A was not changed. Taking everything into consideration, MLCK partially enhances CCE, but suppresses AA-induced Ca2+ entry, i.e. NCCE. MLCK is probably present in the vicinity of PKA and is presumed to have a cooerative effect on the PKA response against CCE and NCCE.</p>

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