Abstract
In this study, we investigated the response of irradiated bone marrow cells to granulocyte colony-stimulating factor (G-CSF). Freshly harvested bone marrow cells were treated with either saline (vehicle control) or 20 ng/ml of G-CSF. Thereafter, cells were separated into nonirradiated (no-IR) and irradiated (IR, 0.5 Gy) groups. IR cells exhibited a higher proliferation rate in response to G-CSF, as compared to the no-IR cells. Reduced levels of reactive oxygen species indicated that G-CSF-treated IR cells produced fewer free radicals, as compared to the no-IR cells. The G-CSF-treated IR cells also had a lower apoptotic rate than their no-IR counterparts. Furthermore, G-CSF-treated IR cells exhibited less alteration of mitochondrial membrane potential, as compared to the no-IR cells. Finally, the mitochondrial number increased in the G-CSF-treated IR cells. The radiation-induced increase in plasma IL-6 in vivo could be enhanced by the administration of G-CSF. The data suggest that radiation potentiates the response of bone marrow cells to G-CSF treatment.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
References
Sloand EM, Yong AS, Ramkissoon S et al (2006) Granulocyte colony-stimulating factor preferentially stimulates proliferation of monosomy 7 cells bearing the isoform IV receptor. Proc Natl Acad Sci USA 103(39):14483–14488
Sultana TA, Harada H, Ito K, Tanaka H, Kyo T, Kimura A (2003) Expression and functional analysis of granulocyte colony-stimulating factor receptors on CD34++ cells in patients with myelodysplastic syndrome (MDS) and MDS-acute myeloid leukaemia. Br J Haematol 121(1): 63–75
Marino VJ, Roguin LP (2008) The granulocyte colony stimulating factor (G-CSF) activates Jak/STAT and MAPK pathways in a trophoblastic cell line. J Cell Biochem 103(5): 1512–1523
Wang L, Kurosaki T, Corey SJ (2007) Engagement of the B-cell antigen receptor activates STAT through Lyn in a Jak-independent pathway. Oncogene 26(20):2851–2859
Gits J, van Leeuwen D, Carroll HP, Touw IP, Ward AC (2006) Multiple pathways contribute to the hyperproliferative responses from truncated granulocyte colony-stimulating factor receptors. Leukemia 20(12):2111–2118
Thummasorn S, Kumfu S, Chattipakorn S, Chattipakorn N (2011) Granulocyte-colony stimulating factor attenuates mitochondrial dysfunction induced by oxidative stress in cardiac mitochondria. Mitochondrion 11(3):457–466
Harada M, Qin Y, Takano H et al (2005) G-CSF prevents cardiac remodeling after myocardial infarction by activating the Jak-Stat pathway in cardiomyocytes. Nat Med 11(3):305–311
Lotem J, Sachs L (1993) Hematopoietic cells from mice deficient in wild-type p53 are more resistant to induction of apoptosis by some agents. Blood 82(4):1092–1096
van Raam BJ, Drewniak A, Groenewold V, van den Berg TK, Kuijpers TW (2008) Granulocyte colony-stimulating factor delays neutrophil apoptosis by inhibition of calpains upstream of caspase-3. Blood 112(5):2046–2054
Watson RW, O’Neill A, Brannigan AE et al (1999) Regulation of Fas antibody induced neutrophil apoptosis is both caspase and mitochondrial dependent. FEBS Lett 453(1–2):67–71
Tsuji K, Ebihara Y (2001) Expression of G-CSF receptor on myeloid progenitors. Leuk Lymphoma 42(6):1351–1357
Bhattacharyya M, Ghosh MK (2008) Hemophagoctic lymphohistiocytosis–recent concept. J Assoc Physicians India 56:453–457
Author information
Authors and Affiliations
Corresponding author
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 2013 Springer Science+Business Media New York
About this paper
Cite this paper
Zhang, Z. et al. (2013). Radiation Affects the Responsiveness of Bone Marrow to G-CSF. In: Van Huffel, S., Naulaers, G., Caicedo, A., Bruley, D.F., Harrison, D.K. (eds) Oxygen Transport to Tissue XXXV. Advances in Experimental Medicine and Biology, vol 789. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-7411-1_37
Download citation
DOI: https://doi.org/10.1007/978-1-4614-7411-1_37
Published:
Publisher Name: Springer, New York, NY
Print ISBN: 978-1-4614-7256-8
Online ISBN: 978-1-4614-7411-1
eBook Packages: Biomedical and Life SciencesBiomedical and Life Sciences (R0)