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Biology

Jim Windelborn

Assistant Professor of Biology
Education

B.S. in Cell and Structural Biology. University of Illinois, Urbana-Champaign. 2000.

Ph.D. in Neuroscience. University of Wisconsin, Madison. 2007.

Research

Dr. Windelborn has studied the cellular and molecular bases of neurologic traumas and neuromuscular diseases. Models used in his research include acute brain slices and mammalian cell cultures.

As an example of research performed in the Windelborn lab, students explore the cellular and molecular mechanisms of damage caused by cerebral ischemia, a condition commonly caused by stroke. Stroke afflicts almost 800,000 Americans each year. Of those, approximately 15% will die from the acute symptoms of the incident. The remaining 85% of stroke victims will survive, but many will be left with deficiencies and disabilities that impact quality of life and impose high economic costs on society. Unfortunately, our understanding of the mechanisms underlying cerebral ischemic damage has not yet yielded broadly effective treatments. A better understanding of these mechanisms will increase potential therapeutic targets and help to reduce the impact stroke has on the lives of its victims and their caretakers.

One relatively unexplored cause of neuronal damage is the lysosome. This cellular organelle is vital for recycling of cellular components and for destruction of pathogens. However, recent evidence has shown that lysosomes become permeabilized following ischemia, allowing normally sequestered catabolic enzymes to escape into the cytoplasm. This can lead to widespread destruction of vital structural and enzymatic cellular components. My laboratory uses a variety of biochemical, cellular and molecular techniques to explore the steps leading to lysosomal membrane permeabilization as well as the contribution of the lysosome to neuronal damage caused by ischemia. 
Pyramidal neurons in the mammalian hippocampus are normally large cells with volumes dominated by large, Nissl-light nuclei. However, following in vitro ischemia and reoxygenation (a laboratory model of stroke), the morphology of these hippocampal neurons is drastically altered. This is indicative of neurons undergoing programmed cell death. One of our major goals is to determine how lysosomes contribute to programmed neuronal death following ischemia.Pyramidal neurons in the mammalian hippocampus are normally large cells with volumes dominated by large, Nissl-light nuclei. However, following in vitro ischemia and reoxygenation (a laboratory model of stroke), the morphology of these hippocampal neurons is drastically altered. This is indicative of neurons undergoing programmed cell death. One of our major goals is to determine how lysosomes contribute to programmed neuronal death following ischemia.

For more detailed information on Dr. Windelborn’s research background, please see his published papers.

Teaching

Fall 2015

General Biology I (BIO 111)

Pathophysiology (BIO 394)

 

Other Courses Taught

General Biology II (BIO 112)

Madmen & History Making (GRW 101)

Biochemistry Laboratory (BIO 409)

Cell Signaling (BIO 394)