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Interruption of spinal cord microglial signaling by alpha-2 agonist dexmedetomidine in a murine model of delayed paraplegia  Marshall T. Bell, MD, Viktor.

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Presentation on theme: "Interruption of spinal cord microglial signaling by alpha-2 agonist dexmedetomidine in a murine model of delayed paraplegia  Marshall T. Bell, MD, Viktor."— Presentation transcript:

1 Interruption of spinal cord microglial signaling by alpha-2 agonist dexmedetomidine in a murine model of delayed paraplegia  Marshall T. Bell, MD, Viktor A. Agoston, MD, Kirsten A. Freeman, MD, Ferenc Puskas, MD, PhD, Paco S. Herson, PhD, Joshua Mares, BS, David A. Fullerton, MD, T. Brett Reece, MD  Journal of Vascular Surgery  Volume 59, Issue 4, Pages (April 2014) DOI: /j.jvs Copyright © 2014 Society for Vascular Surgery Terms and Conditions

2 Fig 1 Hindlimb function, as characterized by the Basso Mouse Score, demonstrated a progressive decline in function of ischemia-reperfusion (IR) controls. Mice treated with dexmedetomidine (Dex) had a similar initial decline; however, their function stabilized and was significantly higher (*P < .05) than IR controls from 36 to 60 hours of reperfusion. Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2014 Society for Vascular Surgery Terms and Conditions

3 Fig 2 Representative slices of spinal cords following sham or IR surgery. Images are shown at original magnification ×40 with images in the box at original magnification. Mice treated with dexmedetomidine (IR+Dex) had more normal appearing anterior horn motor neurons with less gray-white matter disruption and fewer inflammatory infiltrates compared with ischemia-reperfusion (IR) controls. Normal appearing anterior horn neurons were quantified by a blinded observer. All mice undergoing IR surgery had significantly less anterior horn neurons (++P < .05) compared with compared with sham mice. Comparison of mice that underwent IR surgery revealed that mice treated with dexmedetomidine (IR+Dex) had a significantly higher quantity of normal anterior horn neurons (*P < .05). Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2014 Society for Vascular Surgery Terms and Conditions

4 Fig 3 Microglia activation 12 hours following IR surgery was depicted by immunofluorescence of spinal cords incubation with anti-ED-1 on Cy3 channel (red) at ×40 magnification. Nuclei are resented by 4′,6-diamidino-2-phenylindole stain in blue with wheat germ agglutinin conjugated flourescein isothiocyanate staining in green for cytoplasm. All tissue incubated with anti-ED-1anti-body had a significant increase in the area of positive stain compared with IgG controls (*P < .05). Mice treated with dexmedetomidine (IR+Dex) had a significant reduction in ED-1 positive microglia compared with ischemia-reperfusion (IR) controls (++P < .05). Quantification for the area of tissue staining positive for anti-ED-1 antibody was performed and shown. Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2014 Society for Vascular Surgery Terms and Conditions

5 Fig 4 Concentrations of cytokines interleukin (IL)-6 and tumor necrosis factor (TNF)-α in spinal cord homogenates at 60 hours of reperfusion are represented. While TNF-α did a show slight decrease with dexmedetomidine treatment, it did not reach statistical significance. Treatment with dexmedetomidine (IR+Dex), however, did result in a significant in concentration of IL-6 compared with ischemia-reperfusion (IR) controls (*P < .05). Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2014 Society for Vascular Surgery Terms and Conditions

6 Fig 5 Following stimulation with lipopolysaccharide (LPS) microglia in both groups had a significant upregulation of activation marker ED-1 (*P > .05) compared with controls. Dexmedetomidine treatment (LPS+Dex) significantly reduced the expression of activation marker ED-1 compared with controls (LPS) (++P < .05). Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2014 Society for Vascular Surgery Terms and Conditions

7 Fig 6 Microglial expression of cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-6 were significantly increased following lipopolysaccharide (LPS) stimulation (*P > .05) compared with controls. Treatment with dexmedetomidine (LPS+Dex) significantly reduced the expression of both cytokines (++P < .05) compared with LPS treatment alone (LPS). Journal of Vascular Surgery  , DOI: ( /j.jvs ) Copyright © 2014 Society for Vascular Surgery Terms and Conditions

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