Michael Chopp wins the Abraham White Scientific Achievement Award
Tuesday, April 8, 2014
Michael Chopp wins the Abraham White Scientific Achievement AwardDistinguished Professor Michael Chopp, of the Department of Physics, has won the prestigious 2014 Abraham White Scientific Achievement Award. Chopp, who performed this research in his laboratory at Henry Ford Hospital, received the honor for his discovery of the role of thymosin beta4 in the treatment of brain injuries and neurodegenerative diseases. The George Washington University presents the Abraham White Scientific Achievement Award annually to honor individuals who have made unique contributions to science and medicine.
One example of Chopp’s research on thymosin beta 4 can be found in his 2010 paper in the leading journal Neuroscience.
DC Morris, M Chopp, L Zhang, M Lu, and ZG Zhang (2010) Thymosin beta 4 improves functional neurological outcome in a rat model of embolic stroke. Neuroscience, Volume 169, Pages 674-682.
Chopp and this colleagues have mentored many recent graduates of the Biomedical Sciences: Medical Physics PhD program. The research was supported by the National Institutes of Health, including Chopp’s Program Project Grant P01NS023393 from the National Institute of Neurological Disorders and Stroke.
Thymosin beta 4 (T beta 4) is a developmentally expressed 43-amino acid peptide that inhibits organization of the actin-cytoskeleton by sequestration of G-actin monomers. T beta 4 improves cardiac function after myocardial infarction in adult mice and promotes healing properties in both dermal and corneal wounds. We tested the hypothesis that T beta 4 improves functional neurological outcome in a rat model of embolic stroke.
Experimental Procedures: Male Wistar rats (n=18) were subjected to embolic middle cerebral artery occlusion (MCAo). T beta 4 (6 mg/kg, IP) was administered 24 h after MCAo and then every 3 days for four additional doses (n=9). Rats treated with saline were used as a control (n=9). The adhesive-removal test (ART) and modified Neurological Severity Score (mNSS) were performed to measure functional outcome. Rats were sacrificed 56 days after MCAo. Immuno-staining was performed with antibodies against NG-2 (chondroitin sulfate proteoglycan), CNPase (2", 3"-cyclic nucleotide 3'-phosphodiesterase) to detect immature and mature oligodendrocytes. Neurofilament-H (NF-H) antibodies were used to detect axons while myelinated axons were identified with Bielschowsky/Luxol (B/L) Blue staining. EBA (endothelial barrier antigen) was used for detection of mature vessels.
Results: Ischemic rats treated with T beta 4 demonstrated a significant overall improvement (P<0.01) in the ART and the mNSS when compared to controls. Significant improvement was observed beginning at 14 and 35 days, respectively. Lesion volumes showed no significant differences between the two groups. Treatment with T beta 4 increased myelinated axons and increased vessel density in the ischemic boundary (P<0.05) and augmented remyelination which was associated with an increase of oligodendrocyte progenitor cells (OPCs) and myelinating oligodendrocytes (P<0.05).
Conclusions: The present study suggests that T beta 4 improves neurological functional outcome after embolic stroke in rats. Axonal remodeling from mobilization of OPCs is proposed as contributing to T beta 4 induced functional improvement.