Xiaowen Bai, MD, PhDXiaowen Bai, MD, PhD

Associate Professor of Anesthesiology and Physiology

Medical College of Wisconsin
Anesthesiology Research
8701 Watertown Plank Road
Milwaukee, WI 53226-0509
(414) 955-5755 | (414) 955-6507 (fax) | xibai@mcw.edu

Faculty Collaboration Database Profile

Dr. Bai received a PhD in Cell Biology from Beijing University in China.  She completed her postdoctoral fellowship in Stem Cells at the University of Texas M.D. Anderson Cancer Center in Houston. Dr. Bai's research interests involve the application of stem cells in tissue regeneration, drug screening, and disease modeling. Currently, she is the Principal Investigator on an NIH R01 grant and the Stem Cell Core Director on an NIH Program Project Grant. Dr. Bai remains a member of several professional societies and serves as an editorial board member for a number of journals including the Journal of Molecular and Cellular Cardiology. The focus of Dr. Bai’s current research is on the following three areas:

Research Area 1: Anesthetic-induced developmental neurotoxicity:
Growing evidence demonstrates that prolonged anesthesia with general anesthetics induces widespread neuronal cell death followed by long-term memory and learning disabilities in animal models, seriously questioning the safety of obstetric and pediatric anesthesia. In addition, the underlying mechanisms of anesthetic neurotoxicity are complex and not well understood. We utilize gain- and loss-of-function approaches to examine the novel molecular mechanisms underlying the roles of microRNAs and mitochondrial dynamics in anesthetic neurotoxicity in mice, and translate the findings to humans using stem cell-derived neurons.

Selected publications:

  1. Twaroski DM, Yan Y, Olson JM, Bosnjak ZJ, Bai X (corresponding author). Down-regulation of miR-21 mediates propofol-induced neurotoxicity in developing human neurons. Anesthesiology, 121(4):786-800, 2014.
  2. Twaroski D, Yan Y, Zaja I, Liu Y, Bosnjak ZJ, Bai X (corresponding author). Inhibition of mitochondrial fission attenuates propofol-induced developmental neurotoxicity in human neurons. Anesthesiology, 123(5):1067-83, 2015.
  3. Twaroski D, Bosnjak ZJ, Bai X (corresponding author). MicroRNAs: new players in anesthetic-induced developmental neurotoxicity. Pharmaceutica Analytica Acta, 6:357, 2015.

Research Area 2: Stem cell-mediated myocardial regeneration:
Myocardial infarction is one of the major causes of death throughout the world. Currently, there is no very effective approach for treatment. Stem cells hold a promise in repairing injured cardiac tissue. Our lab is involved in studying the effect of the transplantation of adipose tissue-derived stem cells and induced pluripotent stem cell-derived cardiomyocytes on myocardial regeneration following ischemia injury. A molecular imaging method has been developed to investigate the molecular mechanisms controlling homing, engraftment, and survival of injected cells in vivo.

Selected publications:

  1. Bai X, Yan Y, Song YH, Rabinovich B, Seidensticker M, Metzele R, Bankson JA, Vykoukal D, Alt E. Both cultured and freshly isolated adipose tissue-derived stem cells enhance cardiac function after acute myocardial infarction. Eur Heart J, 31(4): 489–501, 2010.
  2. Bai X (corresponding author), Alt E. Myocardial regeneration potential of adipose tissue-derived stem cells. Biochem Biophys Res Commun, 401(3):321-6, 2010.
  3. Bai X, Yan Y, Coleman M, Wu G, Rabinovich B, Seidensticker M, Alt E. Tracking long-term survival of intramyocardially delivered human adipose tissue derived stem cells using bioluminescence imaging. Mol Imaging Biol, 13(4):633-45, 2011.
  4. Kikuchi C, Bienengraeber M, Canfield S, Koopmeiners A, Schaefer R, Bosnjak ZJ, Bai X (corresponding author). Comparison of cardiomyocyte differentiation potential of type 1 diabetic donor- and non-diabetic donor-derived induced pluripotent stem cells. Cell Transplant, 24(12):2491-504, 2015.

Research Area 3: The mechanisms of impaired cardioprotection under diabetic conditions:
Hyperglycemia has been shown to be particularly detrimental to the cardioprotective effects provided by anesthetic preconditioning, with the underlying mechanisms remaining largely unknown. We have developed and validated a clinically relevant model of cardiac preconditioning using human cardiomyocytes, derived from both normal induced pluripotent stem cells (iPSCs) and diabetes mellitus iPSCs. This in vitro model of human disease will enable developmental and comparative studies of normal and diabetic cardiomyocytes to address genetic and environmental mechanisms responsible for attenuation of preconditioning efficacy in diabetics.

Selected publications:

  1. Zaja I, Bai X (corresponding author), Liu Y, Kikuchi C, Dosenovic S, Yan Y, Canfield SG, Bosnjak ZJ. Cdk1, PKCδ and calcineurin-mediated Drp1 pathway contributes to mitochondrial fission-induced cardiomyocyte death. Biochem Biophys Res Commun, 453(4):710-721, 2014.
  2. Olson J, Yan Y, Bai X, Liang M, Kriegel A, Bosnjak ZJ. MicroRNA-21 mediates isoflurane-induced cardioprotection through PDCD4, independent of PTEN. Anesthesiology, 122(4):795-805, 2015.
  3. Canfield S, Zaja I, Twaroski D, Bai X (corresponding author), Bosnjak ZJ. High glucose attenuates anesthetic preconditioning in stem cell-derived cardiomyocytes: a role of reactive oxygen species and mitochondrial fission. Anesth Analg, 122(5):1269-79, 2016.

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