PKC activation by melatonin modulates vimentin intermediate filament organization in N1E-115 cells

Authors

  • Gloria Benítez-King

    1. Instituto Mexicano de Psiquiatría, Departamento de Neurofarmacología, DIC, Calz. México-Xochimilco No 101, Col. Sn. Lorenzo Huipulco, México, D.F., CP 14370, México
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Address reprint requests to Dr Gloria Benítez-King, Instituto Mexicano de Psiquiatría, Departamento Neurofarmacología, DIC, Calz. México-Xochimilco No 101, Col. Sn. Lorenzo Huipulco, México, D.F., CP 14370, México.
E-mail: bekin@imp.edu.mx

Abstract

Melatonin enters cells and causes cytoskeletal rearrangements in unicellular organisms, plants and vertebrates. This pineal secretory product causes microtubule enlargement and neurite outgrowth by a calmodulin antagonism in N1E-115 cells. Recently, direct in vitro activation of protein kinase C by melatonin was described. Vimentin intermediate filaments are attached to microtubules and their organization depends on both microtubule distribution and phosphorylation of specific proteins. Protein kinase C is a serine threonine kinase which phosphorylates vimentin and through this mechanism causes intermediate filament disassembly. In this work the effects of melatonin on protein kinase C activation, content, and subcellular distribution were studied in N1E-115 cells. Also, melatonin effects on vimentin phosphorylation and subcellular distribution were explored. The results show that melatonin both activates and increases protein kinase C content in the membrane–cytoskeletal fraction. Melatonin protein kinase C activation was followed by an increase in both vimentin phosphorylation and by vimentin subcellular redistribution. Moreover, staurosporine, a serine threonine kinase inhibitor, prevented increased vimentin phosphorylation elicited by melatonin. Similar effects to those caused by melatonin were obtained with the protein kinase C activator phorbol 12-myristate 13-acetate. Data support the idea that melatonin modulates vimentin organization through protein kinase C activation.

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