Cardiovascular Center

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Martin Bienengraeber, PhD
Assistant Professor for Anesthesiology, and Pharmacology and Toxicology

Phone: 414-456-5690 

 

Mitochondria constitute the core of cellular energy metabolism as the site of the greatest ATP production. In addition, they play an important role in regulating ionic homeostasis of the cell. It has been suggested that mitochondrial dysfunction may be the major cause for tissue injury during cardiac ischemia and reperfusion. On the other hand, they present a valuable target for triggering protective mechanisms. Exposure of the heart to volatile anesthetics like isoflurane before or after an ischemic event helps to maintain cellular and mitochondrial function in the whole heart, in cardiomyocytes and in isolated mitochondria.
One of my research interests revolves around the role of mitochondria as triggers and effectors in protection of the heart from ischemia and stress. We use physiological, pharmacological and molecular techniques as well as proteomics to demonstrate quantifiable alterations in mitochondrial bioenergetics and protein expression during or after exposure to volatile anesthetics. We plan to apply our findings to target potentially protective proteins to mitochondria by overexpression, thereby increasing the cardiomyocytes' resistance against oxidative stress.
In other ongoing or just starting projects, we study the impact of near infrared light (670 nm) on the heart and mitochondria after ischemia. Exposure of the ischemic heart with this light at the time of reperfusion turns out to be protective, and mitochondria may play a crucial role in the mechanism behind this phenomenon. Projects are performed in collaboration with investigators from the Anesthesiology, the Pharmacology and Toxicology and the Physiology department.

Selected Recent Publications

  • Lohr NL, Keszler A, Pratt P, Bienengraeber M, Warltier DC, Hogg N. Enhancement of nitric oxide release from nitrosyl hemoglobin and nitrosyl myoglobin by red/near infrared radiation: Potential role in cardioprotection. J Mol Cell Cardiol 2009,47;256-63.
  • Mio Y, Shim YH, Richards E, Bosnjak ZJ, Paul S. Pagel PS, Bosnjak ZJ, Bienengraeber M. Xenon Preconditioning: Role of Prosurvival Signaling, Mitochondrial Permeability Transition, and Bioenergetics in Rats Anesth Analg 2009, 108;858-66.
  • Zhang R, Mio Y, Pratt PF, Lohr N, Warltier DC, Whelan HT, Zhu D, Jacobs ER, Medhora M, Bienengraeber M. Near infrared light protects cardiomyocytes from hypoxia and reoxygenation injury by a nitric oxide dependent mechanism. J Mol Cell Cardiol, 2009 46; 4-14.
  • Marinovic J, Ljubkovic M, Stadnicka A, Bosnjak ZJ, Bienengraeber M. Role of sarcolemmal ATP-sensitive potassium channel in oxidative stress-induced apoptosis: mitochondrial connection. Am J Physiol Heart Circ Physiol 2008, 294; H1317-H1325.
  • Wan TC, Ge ZD, Tampo A, Mio Y, Bienengraeber MW, Tracey WR, Gross GJ, Kwok WM, Auchampach JA. The A3 adenosine receptor agonist CP-532,903 [N6-(2,5-dichlorobenzyl)-3'-aminoadenosine-5'-N-methylcarboxamide] protects against myocardial ischemia/reperfusion injury via the sarcolemmal ATP-sensitive potassium channel. J Pharmacol Exp Ther 2008, 324: 234-243.
  • Marinovic J, Ljubkovic M, Stadnicka A, Bosnjak ZJ, Bienengraeber M. Role of sarcolemmal ATP-sensitive potassium channel in oxidative stress-induced apoptosis: mitochondrial connection. Am J Physiol Heart Circ Physiol 2008, 294; H1317-25.





 

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