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Shibani S Mukerji Entering Class: 2002
Undergraduate Institution: Yale University Research Interests: Ischemic stroke is one of the leading causes of mortality and severe, long term disability in the US. Clinical stroke treatments remain elusive but improved understanding of activated endogenous mechanisms offer cellular targets that can be utilized for stroke therapy. Our lab has previously shown that the transforming growth factor-beta superfamily member, activin and its activated intracellular signal Smad2/3 increases following the transient middle cerebral occlusion model in adult mice. This suggests that one endogenous response to ischemia is the upregulation of the activin pathway. Our in vitro data reveal that activin is a survival factor for cortical neurons and is neuroprotective in a model of oxidative stress. These findings provide us with a basis to test whether activin has therapeutic value in ischemic stroke in vivo. A second approach to identify molecular targets for therapy is to investigate the cellular pathways activated following by nonlethal hypoxia exposure. Studies in our lab demonstrate that activin mRNA is increased at 1hour after 2 h of 11% hypoxia but is at normal levels at 4 and 24 hours. The temporal dynamics of activin expression is similar to the time course of erythropoietin (Epo) and vascular endothelial growth factor (VEGF) induction following the same hypoxia exposure. Ongoing studies in the lab will test whether the same transcriptional regulators that control Epo and VEGF mRNA levels also controls activin expression in the brain. About me: Comment about the MSTP program:
Featured Publication: Mukerji SS, Rainey RN, Rhodes J, Hall AK. Delayed Activin A administration attenuates tissue death after transient focal cerebral ischemia and is associated with decreased p38 and JNK activation. J Neurochem. 2009 Sep 24. [Epub ahead of print] Additional Publications: Shibani S. Mukerji, Ekaterina A. Katsman, Charles Wilber, Noah A. Haner, Warren R. Selman and Alison K. Hall. (2006) Activin is a neuronal survival factor that is rapidly increased after transient cerebral ischemia and hypoxia in mice. J Cereb Blood Flow Metab. 2007 Jun;27(6):1161-72 Shibani Mukerji and Alison Hall. Activin Induction in Hypoxia and Ischemic Injury (Abstract). Program No. 95.11. 2005 Abstract Viewer/Itinerary Planner. Society of Neuroscience 35th Annual Meeting: Washington, DC. Online. Gerard, E. Tageldin, M. Mukerji, S. and B. Peterson Frontal Grey and White Matter in Tourette Syndrome (Abstract), Presented at Doris Duke Clinical Research Fellowship’s 1st Annual Conference, St. Louis, MO 2002
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