Journal of Alzheimers Disease & Parkinsonism
Open Access

Research Article

Direct Actions of Granulocyte-Colony Stimulating Factor on Human Neuronal and Monocytic Cell Lines

Amanda Pennington^1,2, Vasyl Sava¹, Shijie Song^1,4, Niketa Patel^3,4 and Juan Sanchez-Ramos^1,2,4*

¹Departments of Neurology, University of South Florida, 13220 Laurel Drive, Tampa, Florida, USA

²Molecular Pharmacology and Physiology, University of South Florida, 13220 Laurel Drive, Tampa, Florida, USA

³Molecular Medicine, University of South Florida, 13220 Laurel Drive, Tampa, Florida, USA

⁴James Haley VA Medical Center, University of South Florida, 13220 Laurel Drive, Tampa, Florida, USA

Corresponding Author:

Sanchez-Ramos J
Department of Neurology
University of South Florida
13220 Laurel Drive, Tampa, Florida 33612
E-mail: jsramos@health.usf.edu

Received date: July 19, 2013; Accepted date: August 16, 2013; Published date: August 23, 2013

Citation: Pennington A, Sava V, Song S, Patel N, Sanchez-Ramos J (2013) Direct Actions of Granulocyte-Colony Stimulating Factor on Human Neuronal and Monocytic Cell Lines. J Alzheimers Dis Parkinsonism 3:121. doi: 10.4172/2161-0460.1000121

Copyright: © 2013 Pennington A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Introduction: Granulocyte colony stimulating factor (G-CSF) administration produces beneficial effects in rodent models of stroke, trauma and neurodegenerative diseases by acting on both bone marrow-derived and neuronal cells. The aim of the study was to elucidate cellular mechanism(s) of G-CSF action by direct application to neuronal and monocytic cell lines.

Method: Cell culture models of monocytes (THP-1) and neurons (SH-SY5Y) cells were incubated with G-CSF. The following parameters were measured: G-CSF receptor binding kinetics; DNA synthesis; signal transduction, in particular expression of alternatively spliced protein kinase C (PKCδVIII) and the anti-apoptotic protein Bcl-2; changes in adhesiveness and migratory properties induced by G-CSF in the monocytic cells.

Results: G-CSF receptor binding kinetics in the two lines differed, with Kd in the neuronal line being significantly higher than that of the monocytic cells. Despite higher affinity of G-CSF for receptors on the monocytic cells, G-CSF treatment increased Bcl-2 expression in the neuronal line at lower concentrations than that required in the monocytic cell line. G-CSF did not increase either cellular adhesiveness or migration through a semi-permeable membrane, whereas monocyte chemotactic protein (MCP-1) significantly improved migration.

Conclusions: The cellular and molecular responses to G-CSF treatment of monocytic cells suggest that neither changes in adhesiveness nor migratory capacity are responsible for the beneficial effects of G-CSF administration in models of neurologic diseases. G-CSF induction of anti-apoptotic signaling in neurons is an important component of its neuroprotective effects in models of brain injury.

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