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Molecular mechanisms of muscle aging How does oxidative stress contribute to changes in cell machinery that ultimately cause age-related disease?

Email Dr. Jennifer Klein for more information on joining her research group: jklein@uwlax.edu; Prairie Springs Science Center 4040

Aging is inevitable, but age-related diseases such as Alzheimer's, cardiovascular disease, and cancer significantly impact the healthy years of your life. Aging causes a decline in muscle power and speed due to muscle atrophy and weakness; by the age of 80, humans lose 40% of muscle mass and 50% of muscle power. Many scientists have found evidence that increasing oxidative stress promotes muscle aging, but it isn't clear why this happens.

Our research group is focused on characterizing muscle proteins that that are targets of cellular oxidation and serve to propagate redox signals throughout metabolic and transcriptional networks, orchestrating changes in muscle physiology that ultimately define human healthspan.

Our work often includes using gene-editing techniques to change the DNA sequence encoding muscle proteins so that they are more or less susceptible to oxidation. We use immunofluorescence and live-cell fluorescence imaging to measure cell function. Other molecular techniques used include quantitate PCR to measure gene expression and western blotting to measure protein activation.

Left: Alex Steil is culturing mammalian muscle myoblasts after a round of gene-editing. Alex graduated in 2019 and is now a PhD student at the University of Colorado-Anschutz Medical Campus.

Top Left: Brandon Harris is measuring calcium transients in excited muscle cells. Brandon graduated in 2019 and is now a PhD student at the University of California-Davis. Top Right: Klein research lab summer 2018. Bottom Left: Danny Walgenbach graduate in 2019 and will be attending Medical School in 2020. Bottom Right: Rachel is using fluorescence microscopy to analyze muscle cell differentiation.