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1 Physiology, Temple University School of Medicine, Philadelphia, PA, USA
2 Cardiology, Temple University School of Medicine, Philadelphia, PA, USA
* To whom correspondence should be addressed. E-mail: mautieri{at}temple.edu.
Introduction. Granulocyte-Colony Stimulating Factor (G-CSF) is a lineage-restricted hematopoetic growth factor which stimulates proliferation and maturation of hematopoetic progenitors, and is a known powerful mobilizer of bone-marrow-derived stem cells. Very little has been reported on G-CSF expression and modulation of Vascular Smooth Muscle Cell (VSMC) activation. The purpose of this study is to characterize the expression and effects of G-CSF on primary human VSMC and balloon angioplasty-injured rat carotid arteries. Methods and Results. In cultured human VSMC, G-CSF mRNA and protein expression is induced by several cytokines, the most potent being Fetal calf serum and T lymphocyte conditioned media. G-CSF is not expressed in naive rat carotid arteries, but is induced in neointimal SMC in carotid arteries subject to balloon angioplasty. G-CSF is chemotactic for human VSMC. There is a significant difference between unstimulated cells and those treated with G-CSF at 100 and 1000pg/ml (p<0.01 and 0.05 for three experiments). G-CSF also activates the GTPase Rac1, a regulator of cellular migration in VSMC. Inhibition of Rac1 inhibits G-CSF-driven VSMC migration. Important signal transduction protein kinases, including p44/42 MAPK, AKT, and S6 kinase are also activated in response to G-CSF. Conclusions. This is the first report describing expression of G-CSF in injured arteries and the multiple effects of G-CSF on VSMC activation. Together, it suggests that G-CSF is an important mediator of inflammatory cell-VSMC communication and VSMC autocrine activation, and may be an important mediator of the VSMC response to injury.
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