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Key Dates


  • March 6, 2012 – Online Registration Opens

  • March 12, 2012 – Abstract submission Closes (all abstracts due at this time)

  • March 12, 2012 - New Investigator Award Applications Due

  • April 16, 2012 - Accepted abstracts for Poster Session, New Investigators Announced

  • May 4, 2012 - Hotel Reservations Close

  • May 21, 2012 - Online Registration Closes
Adhesiveness of Aortic Endothelium in Response to High-LET Radiation is Chemokine Dependent

Kiran B. Gupta, University of Alabama at Birmingham 
Saman F. Khaled, University of Alabama at Birmingham 
*Dennis F. Kucik, University of Alabama at Birmingham 
Xing Wu, University of Alabama at Birmingham 
Tao Yu, University of Alabama at Birmingham 

Keywords: atherosclerosis, High LET, Cosmic Radiation, cardiovascular, 56Fe

Exposure to radiation from a variety of terrestrial sources is associated with increased risk of heart disease and stroke, but little is known about the effects of the high-LET heavy ions present in cosmic radiation. We recently demonstrated that one such ion, 56Fe, accelerates atherosclerotic plaque development in the apoE -/- mouse model. The purpose of the current study was to investigate the mechanism at the cellular level. Since radiation also induces vascular inflammation, a possible mechanism for exacerbation of atherosclerosis is an increase in the adhesiveness of vascular endothelial cells, triggering inflammation and pro-atherogenic accumulation of leukocytes. To address this, human aortic endothelial cells (HAECs) were exposed to 0 to 5 Gy 600 MeV 56Fe, followed by measurement of adhesiveness under shear stress. Twenty-four hours after irradiation, HAEC adhesiveness for leukocytes was increased, with a dose dependence similar to that of atherosclerotic changes in the mouse model. Because the adhesion molecule VCAM-1 is critical in development of atherosclerosis, we then investigated the role of endothelial VCAM-1 and its leukocyte receptor, the integrin alpha4beta1. Measurement of VCAM-1 surface expression by flow cytometry demonstrated that radiation-induced adhesiveness was not due to increased VCAM-1. However, antibody blockade of alpha4beta1 on leukocytes abolished the radiation-induced adhesiveness, suggesting involvement of the VCAM-1/alpha4beta1 receptor-ligand pair in the mechanism. Since the leukocyte integrin alpha4beta1 can be activated by chemokines presented on the endothelial cell surface, the effect of pertussis toxin (PTX), an inhibitor of chemokine-mediated integrin activation, was tested. PTX specifically inhibited radiation-induced adhesiveness, with no significant effect on non-irradiated cells. Therefore, high-LET radiation can induce increased adhesiveness of aortic endothelial cells through chemokine-dependent signaling from endothelial cells to leukocytes, even in the absence of increased expression of the adhesion molecules involved. This work was supported by NSBRI through NASA-NCC-9-58 and by NASA grant NNX11AC61G.

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