Acute Brain Injury: Assessing mitochondrial dysfunction and the role of calpain proteases in vitro.
Brian Polster, PhD
Assistant Professor
University of Maryland
School of Medicine
Webinar Abstract:
Small molecule inhibitors of calcium-activated calpain proteases are protective in animal models of stroke and traumatic brain injury. Mitochondria play an integral role in both apoptotic and excitotoxic/necrotic neuronal death. Mitochondrial control of apoptosis is regulated through the release of entrapped cytotoxic proteins (such as cytochrome c and apoptosis-inducing factor) while necrosis is influenced by mitochondrial calcium uptake, ATP-generating capacity, and reactive oxygen species production. We are investigating the relationship between the activation of calpain and mitochondrial dysfunction in models of acute brain injury.
Join us for this 45 minute webinar to learn how we are employing single-cell fluorescence imaging, the XF24 Analyzer, and pharmacological tools to evaluate the interaction between calpain proteases and mitochondrial bioenergetics.
You Will Learn:
- How we use FRET-based imaging approaches to measure the onset of protease activation in intact cells.
- How we simultaneously evaluate changes in membrane potential and intracellular calcium.
- How we use the XF24 Analyzer to directly examine the influence of calpain inhibition on mitochondrial function in cellular models of neuronal injury.
Assay:
Mitochondrial Function: BOFA
Substrate Utilization: Glutamate, Pyruvate
Log In to View Webinar On-Demand.