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  • Title: Inhibition of agonist-induced Ca2+ entry in endothelial cells by myosin light-chain kinase inhibitor.
    Author: Watanabe H, Takahashi R, Zhang XX, Kakizawa H, Hayashi H, Ohno R.
    Journal: Biochem Biophys Res Commun; 1996 Aug 23; 225(3):777-84. PubMed ID: 8780689.
    Abstract:
    Identification of the signal which links the depletion of Ca2+ stores to a Ca2+ entry pathway in the plasma membrane remains to be determined. In the present study, effects of ML-9 and wortmannin, inhibitors of myosin light-chain kinase (MLCK), on agonist-stimulated Ca2+ response were investigated in porcine aortic endothelial cells loaded with the Ca(2+)-sensitive dye fura-2. Bradykinin (BK) caused a rapid increase in [Ca2+]i, followed by a sustained increase due to the influx of Ca2+ from the extracellular space. ML-9 almost completely abolished the sustained increase in [Ca2+]i in BK-stimulated cells, while it did not affect the mobilization of Ca2+ from intracellular stores. ML-9 also abolished the sustained increase in [Ca2+]i caused by thapsigargin. Wortmannin mimicked the effect of ML-9 on the thapsigargin-stimulated Ca2+ response. These findings document for the first time the involvement of MLCK inhibitor in Ca2+ signaling in endothelial cells.
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