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Regulation of the human atrial myosin light chain 1 promoter by Ca²⁺-calmodulin-dependent signaling pathways

Christiane Woischwill^#, Peter Karczewski^#, Holger Bartsch^*, Hans-Peter Luther^*, Monika Kott^#, Hannelore Haase^# and Ingo Morano^#,,1

^# Max-Delbrück-Center for Molecular Medicine, Berlin-Buch;
Johannes-Müller-Institute for Physiology, University Medicine Berline (Charité), Berlin; and
^* Medical Clinic I, Department of Cardiology, University Medicine Berlin (Charité), Berlin, Germany

¹Correspondence: Max-Delbrück-Center for Molecular Medicine, Robert-Rössle-Str. 10, 13122 Berlin-Buch, Germany. E-mail: imorano{at}mdc-berlin.de

We investigated expression regulation of the human atrial myosin light chain 1 (hALC-1) gene using a cardiomyocyte H9c2 cell line stably transfected with a construct consisting of the human ALC-1 promoter cloned in front of the luciferase gene (H9c2T1). H9c2T1 cells were stimulated with vasopressin, which is known to induce cardiomyocyte hypertrophy and to activate a panel of signaling pathways. Those pathways involved in hALC-1 promoter activity regulation were dissected by using pharmacological inhibitor substances. Stimulation with vasopressin was associated with nuclear NFAT translocation and significantly increased human ALC-1 promoter activity. Inhibition of calcineurin by cyclosporin A blocked the effects of vasopressin on ALC-1 promoter activity to 50%. This suggests that the Ca²⁺-calmodulin-calcineurin-NFAT pathway is involved in human ALC-1 promoter activation. However, inhibition of multifunctional Ca²⁺-calmodulin-dependent protein kinases (CaMK) by KN-93 decreased human ALC-1 promoter activity to almost basal levels. CaMK regulation of ALC-1 promoter activity effect could well be mediated by CaMKIV, which accumulated in the nucleus upon vasopressin stimulation. Inhibition of protein kinase C (PKC) isoforms by bisindolylmaleimide had no significant influence on human ALC-1 promoter activity. Thus, our results demonstrate a dominant role of Ca²⁺-calmodulin-dependent signaling pathways in the regulation of human ALC-1 expression.—Woischwill, C., Karczewski, P., Bartsch, H., Luther, H.-P., Kott, M., Haase, H., Morano, I. Regulation of the human atrial myosin light chain 1 promoter by Ca²⁺-calmodulin-dependent signaling pathways.

Key Words: atrial myosin light chain • H9c2 • promoter regulation • Ca²⁺ signaling

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