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Mediators of Inflammation
Volume 2014, Article ID 518265, 8 pages
http://dx.doi.org/10.1155/2014/518265
Research Article

Production of the Growth Factors GM-CSF, G-CSF, and VEGF by Human Peripheral Blood Cells Induced with Metal Complexes of Human Serum γ-Globulin Formed with Copper or Zinc Ions

Laboratory of Cell to Cell Interactions, N.F. Gamaleya Research Institute of Epidemiology and Microbiology, Health Ministry of the Russian Federation, Gamaleya Street 18, Moscow 123098, Russia

Received 31 March 2014; Accepted 20 May 2014; Published 3 July 2014

Academic Editor: Fulvio D’Acquisto

Copyright © 2014 Sergey B. Cheknev et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

As it was established in our previous studies, the proteins of human serum γ-globulin fraction could interact with copper or zinc ions distributed in the periglobular space, form metal complexes, and become able to perform effector functions differing due to the conformational shifts from those mediated by them in native conformation of their Fc regions. In the present work we have evaluated ability of the γ-globulin metal complexes formed with copper or zinc ions in the conditions like to the physiological ones to induce production or to regulate induction in the culture of freshly isolated human peripheral blood cells (PBC) of granulocyte (G) and granulocyte-macrophage (GM) colony-stimulating factors (CSF) as well as of vascular endothelial growth factor (VEGF). The γ-globulin metal complexes formed with both copper and zinc ions were found to similarly reduce production of GM-CSF, G-CSF, and VEGF induced in normal human PBC cultures by the control γ-globulins or by copper and zinc ions used alone. In context of theory and practice of inflammation the properties of the γ-globulin metal complexes might impact the basic knowledge in search of novel approaches to anti-inflammatory drugs development.