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Xiongwen Chen, PhD

Assistant Professor, Physiology

Telephone:  215-707-3542

Laboratory Telephone:  215-707-5711

Fax:  215-707-0170

Office: Medical Research Building Room 816A

Email: xchen001@temple.edu

Department of Physiology

Cardiovascular Research Center

Undergraduate degree, Beijing (China) Agricultural University, Beijing, China, 1994

 

M.S., Beijing (China) Agricultural University, Beijing, China, 1997

 

PhD, Temple University School of Medicine, Philadelphia, PA, 2003

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• Member, Biophysical Society, 1999-present
• Premium member, American Heart Association, 2000-present
• Heart Failure Society of America, 2006-present
• Leadership Committee, Basic Science Council, American Heart Association, 2007-present
• Spring 2008 American Heart Association Molecular Signaling I Region I Study Group, 2007-2008

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The research interest in my laboratory is the role of calcium ions in the pathogenesis of cardiac disease. The development of heart disease is a complicated process, involving many alterations at the molecular, cellular and whole animal levels. It is well known that calcium ions play very important roles in normal physiology of the heart. Calcium is the key determinant of the contractility of cardiac myocytes and thus the heart contractility. Recently, roles of calcium as a signaling ion have been widely studied. Specifically in the heart, calcium plays roles in cardiac myocyte hypertrophy, death, arrhythmogenic activities and remodeling. However, it is not fully explored that how Ca2+ signaling is encoded among constant change of cytosolic Ca2+ during each heart beat. Currently, I am studying the roles of the L-type calcium channel in heart disease progression with a transgenic mouse model cardiac specifically overexpressing the L-type calcium channel beta2a subunit in collaboration with Drs. Steven R. Houser and Jeffrey Molkentin’s groups with the support from NIH/NHLBI and American Heart Association. The roles of calcium ions in the development of cardiac failure, arrhythmia, hypertrophy, myocyte death, and turnover are under exploration in this model. Techniques used in my laboratory range from molecules to whole animals and include molecular biology, myocyte isolation and culture, electrophysiology, intracellular ion measurements, histology, immunocytochemistry, echocardiography, animal surgeries (transaortic constriction, osmotic minipump implantation, coronary artery ligation), and telemetrical ECG recording.

The ultimate goal of my research is to offer new insights into the physiology and pathophysiology of the heart and help the development of new strategies and drugs for cardiac disease treatment.

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Recent Medically Related Publications, Obtained from PubMed (Click on PubMed ID to view abstract)

19608982. MacDonnell SM, Weisser-Thomas J, Kubo H, Hanscome M, Liu Q, Jaleel N, Berretta R, Chen X, Brown JH, Sabri AK, Molkentin JD, Houser SR, CaMKII negatively regulates calcineurin-NFAT signaling in cardiac myocytes. Circ Res 105:4(316-25)2009 Aug 14

18832749. Jaleel N, Nakayama H, Chen X, Kubo H, MacDonnell S, Zhang H, Berretta R, Robbins J, Cribbs L, Molkentin JD, Houser SR, Ca2+ influx through T- and L-type Ca2+ channels have different effects on myocyte contractility and induce unique cardiac phenotypes. Circ Res 103:10(1109-19)2008 Nov 7

18388322. MacDonnell SM, García-Rivas G, Scherman JA, Kubo H, Chen X, Valdivia H, Houser SR, Adrenergic regulation of cardiac contractility does not involve phosphorylation of the cardiac ryanodine receptor at serine 2808. Circ Res 102:8(e65-72)2008 Apr 25

18359894. Chen X, Zhang X, Harris DM, Piacentino V 3rd, Berretta RM, Margulies KB, Houser SR, Reduced effects of BAY K 8644 on L-type Ca2+ current in failing human cardiac myocytes are related to abnormal adrenergic regulation. Am J Physiol Heart Circ Physiol 294:5(H2257-67)2008 May

17827263. MacDonnell SM, Kubo H, Harris DM, Chen X, Berretta R, Barbe MF, Kolwicz S, Reger PO, Eckhart A, Renna BF, Koch WJ, Houser SR, Libonati JR, Calcineurin inhibition normalizes beta-adrenergic responsiveness in the spontaneously hypertensive rat. Am J Physiol Heart Circ Physiol 293:5(H3122-9)2007 Nov

17272809. Chen X, Wilson RM, Kubo H, Berretta RM, Harris DM, Zhang X, Jaleel N, MacDonnell SM, Bearzi C, Tillmanns J, Trofimova I, Hosoda T, Mosna F, Cribbs L, Leri A, Kajstura J, Anversa P, Houser SR, Adolescent feline heart contains a population of small, proliferative ventricular myocytes with immature physiological properties. Circ Res 100:4(536-44)2007 Mar 2

17092992. Litvin J, Chen X, Keleman S, Zhu S, Autieri M, Expression and function of periostin-like factor in vascular smooth muscle cells. Am J Physiol Cell Physiol 292:5(C1672-80)2007 May

17012360. Mills GD, Harris DM, Chen X, Houser SR, Intracellular sodium determines frequency-dependent alterations in contractility in hypertrophied feline ventricular myocytes. Am J Physiol Heart Circ Physiol 292:2(H1129-38)2007 Feb

16210547. Chen X, Zhang X, Kubo H, Harris DM, Mills GD, Moyer J, Berretta R, Potts ST, Marsh JD, Houser SR, Ca2+ influx-induced sarcoplasmic reticulum Ca2+ overload causes mitochondrial-dependent apoptosis in ventricular myocytes. Circ Res 97:10(1009-17)2005 Nov 11

15922740. Autieri MV, Chen X, The ability of AIF-1 to activate human vascular smooth muscle cells is lost by mutations in the EF-hand calcium-binding region. Exp Cell Res 307:1(204-11)2005 Jul 1

15705962. Harris DM, Mills GD, Chen X, Kubo H, Berretta RM, Votaw VS, Santana LF, Houser SR, Alterations in early action potential repolarization causes localized failure of sarcoplasmic reticulum Ca2+ release. Circ Res 96:5(543-50)2005 Mar 18

15385271. Chen X, Kelemen SE, Autieri MV, Expression of granulocyte colony-stimulating factor is induced in injured rat carotid arteries and mediates vascular smooth muscle cell migration. Am J Physiol Cell Physiol 288:1(C81-8)2005 Jan

15117732. Chen X, Kelemen SE, Autieri MV, AIF-1 expression modulates proliferation of human vascular smooth muscle cells by autocrine expression of G-CSF. Arterioscler Thromb Vasc Biol 24:7(1217-22)2004 Jul

12600875. Piacentino V 3rd, Weber CR, Chen X, Weisser-Thomas J, Margulies KB, Bers DM, Houser SR, Cellular basis of abnormal calcium transients of failing human ventricular myocytes. Circ Res 92:6(651-8)2003 Apr 4

12242270. Chen X, Piacentino V 3rd, Furukawa S, Goldman B, Margulies KB, Houser SR, L-type Ca2+ channel density and regulation are altered in failing human ventricular myocytes and recover after support with mechanical assist devices. Circ Res 91:6(517-24)2002 Sep 20

10888251. Yang Y, Chen X, Margulies K, Jeevanandam V, Pollack P, Bailey BA, Houser SR, L-type Ca2+ channel alpha 1c subunit isoform switching in failing human ventricular myocardium. J Mol Cell Cardiol 32:6(973-84)2000 Jun

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• Jay N. Cohn New Investigator Award, HFSA 2007
• Melvin L. Marcus Young Investigator Award in Cardiovascular Sciences Finalist, Winner, American Heart Association 2006
• Young Investigator Award, American Heart Association, 2002
• Best Poster Award of XVII World Congress of International Society for Heart Research, 2001
• University Fellowship, Temple University, 1997-1999
  

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Dr. Chen's lab is located MRB 816    215-707-5711

Postdoctoral Fellows:

Xiaoying (Michelle) Zhang - xiaoying.zhang@temple.edu

 

Graduate Students:

Yingxin Li - yingxin.li@temple.edu

Yinzheng Guan - yinzheng.guan@temple.edu

 

Laboratory Technician/Manager:

Mingxin Tang, MD - mingxin.tang@temple.edu

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Active Support
As Principal Investigator:
Ca2+-influx Induced Cardiac Hypertrophy, Arrhythmia, and Myocyte
Apoptosis
AHA Scientist Development Grant: 0730347N
Total award, direct costs: $260,000 2007-2011
As Principal Investigator:
1 R01 HL088243-01
Ca2+-Influx Regulated Cardiac Hypertrophy, Arrhythmia and
Myocyte Apoptosis
Total award, direct costs: $1,250,000 2007-2012

Previous Support
As Principal Investigator:
0110091U
American Heart Association Predoctoral Fellowship Grant
Does Hyperphosphorylation of L-type Calcium Channel and Ryanodine
Receptor Contribute to the Altered E-C Coupling in Failing Hearts?
2001-03

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