Xun Ai, M.D.

Assistant Professor

Professional Background
B.S./M.D., Medicine
Suzhou Medical College (now Soochow University), China 1985

M.S., Medical Science
Shanghai Medical University (now Fudan University). China 1996

Postdoctoral Training,
Johns Hopkins University / University of Illinois at Chicago 


Ai Lab Members
Weiwei Zhao – Research Assistant
Justin K Thomson – Research Assistant

Xiaomin Wu Ph.D. - Post-Doctoral Fellow
Jiajie Yan M.S. – PhD student

WeiWei Zhao - Research Assistant
  

Our Research
Our research is focused on understanding the mechanisms of cardiac arrhythmias, especially atrial fibrillation (AF) in the aging heart per se and in the aged heart with co-existing cardiovascular diseases. We recently discovered that c-jun N terminal kinase (JNK) plays a critical role in atrial gap junctional remodeling and atrial arrhythmia development in aged atria. With grant support from the NIH and American Heart Association, we are conducting exciting research that will substantially increase our understanding of JNK signaling as a critical contributor to arrhythmia development in aged atria. Our current research focus will help us to achieve our long-term goal to further understand the relationship between aging and co-existing cardiovascular disease in the development of AF and, ultimately to develop novel and effective therapeutic strategies for AF prevention and treatment in the elderly.

In addition to our expertise on molecular biochemistry techniques, we have established many cutting-edge electrophysiological techniques including:

  1. Optical mapping calcium transients (Ca) and action potentials (AP) simultaneously in intact hearts,
  2. Using two-photon microscopy to obtain super-resolution images of Ca / AP and define myocardial and interstitial matrix structure in the same intact hearts,
  3. in vivo/ex vivo cardiac arrhythmia induction.
  4. Measuring intercellular resistivity using a novel 4-electrode microimpedance technique in intact hearts

 

 

Movie 1: An example of uniformly propagated action potentials in a sham-control atrial monolayer.

Movie 2: An example of reentrant action potential propagation in JNK activated atrial monolayers.

Movie 3: An example of uniformly propagated action potentials in a JNK activated atrail monolayer with subsequent overexpressed exogenous wild-type Cx43 (active Cx43).

Movie 4: An example of reentrant action potential propagation in a JNK activated atrial monolayer with subsequent overexpressed exogenous dominant-negative Cx43 (inactive Cx43).

Select Publications

Wang Y, Du Y, Ai X. Cardiac Electrophysiology: A Challenging and Fast Progressing Field. The Scientific World Journal 2013, In Press

Yan J, Kong W, Zhang Q, Beyer EC, Walcott G, Fast VG, Ai X. c-Jun N-terminal kinase activation contributes to reduced Cx43 and atrial arrhythmia development in the aged rabbit left atria. Cardiovascular Res 2013, 97(3):589-97. PMID:23241357

Zhu Y, Ai X, Oster RA, Bers DM, Pogwizd SM. Sex differences in repolarization and slow delayed rectifier potassium current and their regulation by sympathetic Stimulation in rabbits. Pflugers Arch 2012,465(6)805-18. PMID:23242028

Respress JL, van Oort RJ, Li N, Rolim N, Dixit S, Voigt N, Lawrence WS, Skapura DG, Wisloff U, Wieland T, Ai X, Pogwizd SM, Dobrev D, Wehrens XHT. Role of RyR2 Phosphorylation at S2814 during Heart Failure Progression. Circ Res 2012, 110(11):1474-83. PMID:22511749

Ai X, Jiang A, Ke Y, Solaro JR, Pogwizd SM. Enhanced expression of p21-activated kinases in an arrhythmogenic rabbit model of heart failure contributes to dephosphorylation of connexin 43. Cardiovasc Res, 2011, 92(1):106-14. PMID:21727092

Ai X (Corresponding Author), Zhao W, Pogwizd SM. Connexin 43 knockdown or overexpression modulates cell coupling in control and failing rabbit left ventricular myocytes.  Cardiovasc Res 2010 Mar 1;85(4):751-62. PMID: 19880431

DeSantiago J, Ai X, Islam M, Acuna G, Ziolo MT, Bers DM, Pogwizd SM. Arrhythmogenic effects of b2-adrenergic stimulation in the failing heart are due to enhanced SR Ca load. Circ Res 2008;102:1389-97. PMCID: PMC2585979

Fahrenbach J, Ai X, Banach K. Decreased intercellular coupling improves the function of cardiac pacemakers derived from mouse embryonic stem cells. J  Mole Cell Cardiol 2008;45(5):642-9. PMID: 18817780

Other Publications

 Conference Presentations

“JNK2 impairs atrial conduction and enhances arrhythmogenicity in mouse atria.” Poster Presentation at the Basic Cardiovascular Science 2013 Scientific Sessions. Yan J (New Investigator Travel Award Winner), Zhao W, Tong M, Zhang Q, Fast VG, Prabhu SD, Ai X.

“The c-Jun N-terminal kinase activation contributes to reduced connexin43 and atrial fibrillation development in rabbit atrium in vivo”, Poster Presentation at 33rd Heart Rhythm Society Annual Meeting, 2012, Zhang Q, Yan J, Walcott G, Ai X..

“The c-Jun N-terminal kinase activation contributes to reduced connexin43 and atrial fibrillation development in atrial monolayers”, Poster Presentation at 32nd Heart Rhythm Society Annual Meeting, 2011, Yan J, Zhao W, Ai X.

“Connexin 43 downregulation and slowing of conduction are associated with increased inducibility of atrial arrhythmias in the aged rabbit left atrium”, Feature Poster Presentation at 31st Heart Rhythm Society Annual Meeting, 2010. Kong W, Yan J, Zhao W, Li L, Fast VG, Ai X.

Open Position

The Cell and Molecular Physiology Department in the Stritch School of Medicine in the Health Sciences Division at Loyola University Chicago is seeking a highly motivated post-doctoral research fellow who has training in electrophysiology and/or biomedical engineering to contribute to studies of stress signaling regulated electrophysiological remodeling in atrial fibrillation development.  This NIH-funded project involves calcium imaging and action potential recording in intact heart tissue using optical mapping, two-photon intravital imaging techniques.  Our research focus is to understand the mechanisms of cardiac arrhythmias, especially atrial fibrillation (AF) in the aging heart per se and in the aged heart with co-existing cardiovascular diseases using combined molecular biochemical techniques and cutting edge electrophysiological approaches. 

Qualified candidates must hold a Ph.D. or equivalent degree with training in electrophysiology, biomedical engineering, or other relevant field.  Experience with calcium imaging and optical mapping is preferred.  Applicants should email a cover letter describing scientific interests, CV and names of three references with contact information to:  xai1@lumc.edu.

Loyola University Chicago is an Equal Opportunity/Affirmative Action Employer.