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Welcome to the Halterman Lab
Molecular-Based Therapies for Ischemic Brain Injury
We are interested in finding new approaches to treat ischemic brain injury. In particular, our lab focuses on signaling nodes in transcriptional networks that regulate neuron survival and are amenable to small molecule regulation. Putative targets identified through genomic and proteomic-based screens are first validated in vivo and studied further using primary neuronal cultures, neurospheres and related in vitro assays. To manipulate gene function we use several complementary approaches including knockout mouse models, viral mediated gene regulation, site-directed mutagenesis and pharmacological inhibition. Ultimately, our goal is to identify novel therapeutic targets and treatments for disorders in which ischemia is a central component.
Control (left) and ischemia-induced nuclear condensation (right) in neurons of the CA1 field of the hippocampus following 25 minutes bilateral carotid occlusion. Sections were stained with Hoechst and imaged using optical sectioning microscopy. Nuclear area was measured directly in ImageJ.
Corresponding frequency distributions of nuclear area (µm2). Normal curves were fit through method of least squares, constrained by a SD of 15 or less.
Doublestaining of the LysGFPknock mouse cortex with PECAM for blood vessels(red), Laminin, for basal lamina(blue) Neutrophils(green). Notice the perivascular machrophages that line the small blood vessels in brain. Magn. 40x
Showing 2 of 32 journal articles.
Rininger A; Wayland A; Prifti V; Halterman MW. "Assessment of CA1 injury after global ischemia using supervised 2D analyses of nuclear pyknosis." Journal of neuroscience methods. 2012; 207(2):181-8. Epub 2012 Apr 21.
Rininger A; Dejesus C; Totten A; Wayland A; Halterman MW. "MKP-1 antagonizes C/EBP? activity and lowers the apoptotic threshold after ischemic injury." Cell death and differentiation. 2012; 19(10):1634-43. Epub 2012 Apr 20.