Neuroscience 2005 Abstract
Presentation Number: | 99.10 |
---|---|
Abstract Title: | Human umbilical cord blood cells rescue infarct core. |
Authors: |
Newcomb, J. D.*1,2
; Ajmo, JR, C. T.3
; Collier, L. A.3
; Davis Sanberg, C.4
; Pennypacker, K. R.3
; Sanberg, P. R.1,2,4
; Willing, A. E.1,2
1Center of Excellence for Aging and Brain Repair, Univ. of South Florida, Tampa, FL 2Neurosurgery, Univ. of South Florida, Tampa, FL 3Pharmacology, Univ. of South Florida, Tampa, FL 4FL, 12901 Bruce B Downs, 33612, |
Primary Theme and Topics |
Disorders of the Nervous System - Ischemia -- Neuroprotection and tolerance |
Secondary Theme and Topics | Disorders of the Nervous System<br />- Neurotoxicity, Inflammation, and Neuroprotection<br />-- Neuroprotective mechanisms and treatments |
Session: |
99. Hypoxia/Ischemia: Neurogenesis and Stem Cells Poster |
Presentation Time: | Saturday, November 12, 2005 2:00 PM-3:00 PM |
Location: | Washington Convention Center - Hall A-C, Board # SS86 |
Keywords: | ISCHEMIA, INFLAMMATION, TRANSPLANTATION, TIMING |
The ischemic core is believed to lose cells through necrosis initiated at the onset of embolic stroke. Hence, the vast majority of stroke research has only focused on arresting the spread of neuronal death by rescuing cells in the penumbra which die more slowly through apoptosis. Our lab has successfully limited infarct progression and boosted behavioral recovery by treating the middle cerebral artery occluded (MCAO) rat model of stroke with i.v. administered human umbilical cord blood cells (HUCBC). Recently, we found that the majority of animals treated with HUCBC 48 hrs following MCAO fully recovered, (Newcomb et al., SFN, 2004), challenging the notion that cells in the core are necrotic and beyond therapeutic intervention. In the present study we reproduced these findings and extended our description of cell death and inflammation after MCAO and HUCBC transplantation. Sixty-three male Sprague-Dawley rats were randomly distributed into three groups (Sham, MCAO only and MCAO + HUCBC). Loss of cerebral blood flow was monitored using laser Doppler and criterion for inclusion after permanent insertion of an embolus was set at 75% drop in cerebral blood pressure. The rats were sacrificed at various time points following MCAO and biochemical and histological analysis performed on the harvested brains, spleens and thymus to measure infarct volume and activation of inflammatory signals. Our results indicate that HUCBC, when given 48 hrs after stroke, reduces the inflammatory response providing neuroprotection and leading to physiological recovery. These results suggest HUCBC could, potentially lead to therapies that would allow a greater number of stroke victims to receive treatment who otherwise wouldn’t fit the current therapeutic criteria.
Supported by This work was supported by the AHA grant (#0355183B to AEW). PRS is cofounder and AEW and CDS are consultants to Saneron CCEL Therapeutics, Inc.
<B>Conflict of Interest:</B> PRS is cofounder and AEW and CDS are consultants to Saneron CCEL Therapeutics, Inc.
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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