David Stowe, MD, PhD
Professor
Contact Information
Education
Diploma, Zoology, Free University of Berlin - Berlin, Germany, 1966
BA, Zoology, Indiana University - Bloomington, IN, 1968
MA, Cell Biology, Indiana University - Bloomington, IN, 1970
PhD, Physiology, Michigan State University - East Lansing, MI, 1974
Postdoc, Cardiac Physiology, University of California - San Francisco, CA, 1974–1976
MD, Medical College of Wisconsin - Milwaukee, WI, 1979-1983
Residency, Anesthesiology, Medical College of Wisconsin - Milwaukee, WI, 1983–1987
BA, Zoology, Indiana University - Bloomington, IN, 1968
MA, Cell Biology, Indiana University - Bloomington, IN, 1970
PhD, Physiology, Michigan State University - East Lansing, MI, 1974
Postdoc, Cardiac Physiology, University of California - San Francisco, CA, 1974–1976
MD, Medical College of Wisconsin - Milwaukee, WI, 1979-1983
Residency, Anesthesiology, Medical College of Wisconsin - Milwaukee, WI, 1983–1987
Research Interests
- Mechanisms for and protection against cardiac ischemia-reperfusion injury
- Identification and function of mitochondrial ion channels and ion exchangers
- Assessment of mitochondrial transmembrane calcium fluxes and sequestration
- Mitochondrial protection against subacute liver ischemia and traumatic brain injury
The Stowe laboratory is currently active in several areas:
- Mechanism and timing of activation of cardiac mitochondrial small and large K+-sensitive Ca2+ (SKCa and BKCa) channels; their protective role against acute cardiac injury; identification of specific mitochondrial SKCa splice variants in several species, including human; and the molecular and biophysical mechanisms underlying protection by opening of these mitochondrial channels.
- Mitigation of Ca2+ dysregulation and excess reactive oxygen species emission in acute cardiac injury.
- Regulation of mitochondrial Ca2+ flux through Ca2+ channels and Ca2+ exchangers with H+, K+ and Na+; and exploration of dynamic mitochondrial Ca2+ buffering mechanisms.
- Ischemia-induced nitration of nucleotide transporters VDAC and ANT on promoting mitochondrial and cell damage with identification of specific residues that are causative in impeding nucleotide transport and mitochondrial dysfunction.
- Mitochondrial function in liver cells during the perioperative transplant period.
- Mitochondrial function in glial and neurons after subacute tramatic brain injury.
Collaborators include: AKS Camara, WM Kwok, C Pawela, A Geurts, J Hong, MY Yang, J Mishra, Q Cheng, L Keguo, JS Heisner, D Schwabe, and pre- and post doctoral students.