Ching-Pin Chang

Honors and Awards

• New Faculty Award, California Institute of Regenerative Medicine (2008-2013)
• March of Dimes Research Program Award, March of Dimes Foundation (2007-2010)
• Medical Grant Award, Children's Heart Foundation (2007)
• Faculty Scholar Award, Donald E. and Delia B. Baxter Foundation (2006)
• National Scientist Development Award, American Heart Association (2005)
• Research Incentive Award, Office of Technology and Licensing, Stanford University (2005)
• Weinstein Award, Weinstein Cardiovascular Development Conference (2005)
• Keystone Symposia Scholarship, Keystone Symposia for “Molecular Biology of Heart Disease and Cardiac Development" (2004)
• Physician-Scientist Fellowship Award, Howard Hughes Medical Institute (2001-2004)

Professional Education

• Physician-Scientist Fellowship, Howard Hughes Medical Institute Cardiovascular Development (2004)
• Cardiology Fellowship, Stanford University Medical Center Clinical Cardiology (2001)
• Residency, Massachusetts General Hospital, Harvard Internal Medicine (1999)
• Ph.D., Stanford University Cancer Biology (1997)
• M.D., National Taiwan University Medicine

Postdoctoral Advisees

• Pei Han, Wei Li, Chien-Jung Lin, Ching Shang, Yiqin Xiong, Jin Yang

Graduate & Fellowship Program Affiliations

• Cancer Biology
• Medicine

Web Site Links

• My Lab Site

Research Interests

My laboratory studies the mechanisms of cardiovascular development, particularly how the three major types of cardiac cells (endocardial, myocardial and epicardial cells) and neural crest cells interact with each other to generate heart tissues. We are interested in the transcriptional and signaling events that coordinate their interactions and assembly into heart tissues. The long-term goal is to understand the developmental mechanisms that control tissue formation and recapitulate the developmental processes for therapeutic or regenerative purposes. Furthermore, we have generated mouse models of cardiomyopathy and models that allow us to study the repair mechanisms of vascular injury in adult. We aim to applying lessons learned from our developmental studies to investigating the mechanisms of adult disease.

Publications

• Endocardial Brg1 represses ADAMTS1 to maintain the microenvironment for myocardial morphogenesis. Stankunas K,  Hang CT, Tsun ZY, Chen H, Lee NV, Wu JI, Shang C, Bayle JH, Shou W, Iruela-Arispe ML, Chang CP.  Dev Cell.  2008; 14 (2): 298-311
• NFAT dysregulation by increased dosage of DSCR1 and DYRK1A on chromosome 21. Arron JR,  Winslow MM, Polleri A, Chang CP, Wu H, Gao X, Neilson JR, Chen L, Heit JJ, Kim SK, Yamasaki N, Miyakawa T, Francke U, Graef IA, Crabtree GR.  Nature.  2006; 441 (7093): 595-600
• A field of myocardial-endocardial NFAT signaling underlies heart valve morphogenesis. Chang CP,  Neilson JR, Bayle JH, Gestwicki JE, Kuo A, Stankunas K, Graef IA, Crabtree GR.  Cell.  2004; 118 (5): 649-63
• Structure of a HoxB1-Pbx1 heterodimer bound to DNA: role of the hexapeptide and a fourth homeodomain helix in complex formation. Piper DE,  Batchelor AH, Chang CP, Cleary ML, Wolberger C.  Cell.  1999; 96 (4): 587-97
• Meis proteins are major in vivo DNA binding partners for wild-type but not chimeric Pbx proteins. Chang CP,  Jacobs Y, Nakamura T, Jenkins NA, Copeland NG, Cleary ML.  Mol Cell Biol.  1997; 17 (10): 5679-87
• Pbx proteins display hexapeptide-dependent cooperative DNA binding with a subset of Hox proteins. Chang CP,  Shen WF, Rozenfeld S, Lawrence HJ, Largman C, Cleary ML.  Genes Dev.  1995; 9 (6): 663-74
• Calcineurin/NFAT signaling is required for neuregulin-regulated Schwann cell differentiation. Kao SC,  Wu H, Xie J, Chang CP, Ranish JA, Graef IA, Crabtree GR.  Science.  2009; 323 (5914): 651-4
• SM22alpha-targeted deletion of bone morphogenetic protein receptor 1A in mice impairs cardiac and vascular development, and influences organogenesis. El-Bizri N,  Guignabert C, Wang L, Cheng A, Stankunas K, Chang CP, Mishina Y, Rabinovitch M.  Development.  2008; 135 (17): 2981-91
• Pbx1 functions in distinct regulatory networks to pattern the great arteries and cardiac outflow tract. Chang CP,  Stankunas K, Shang C, Kao SC, Twu KY, Cleary ML.  Development.  2008; 135 (21): 3577-86
• Pbx/Meis deficiencies demonstrate multigenetic origins of congenital heart disease. Stankunas K,  Shang C, Twu KY, Kao SC, Jenkins NA, Copeland NG, Sanyal M, Selleri L, Cleary ML, Chang CP.  Circ Res.  2008; 103 (7): 702-9
• Down syndrome critical region-1 is a transcriptional target of nuclear factor of activated T cells-c1 within the endocardium during heart development. Wu H,  Kao SC, Barrientos T, Baldwin SH, Olson EN, Crabtree GR, Zhou B, Chang CP.  J Biol Chem.  2007; 282 (42): 30673-9
• Smad signaling in the neural crest regulates cardiac outflow tract remodeling through cell autonomous and non-cell autonomous effects. Jia Q,  McDill BW, Li SZ, Deng C, Chang CP, Chen F.  Dev Biol.  2007; 311 (1): 172-84
• Molecular imaging of bone marrow mononuclear cell homing and engraftment in ischemic myocardium. Sheikh AY,  Lin SA, Cao F, Cao Y, van der Bogt KE, Chu P, Chang CP, Contag CH, Robbins RC, Wu JC.  Stem Cells.  2007; 25 (10): 2677-84
• Myocardial restoration with embryonic stem cell bioartificial tissue transplantation. Kofidis T,  de Bruin JL, Hoyt G, Ho Y, Tanaka M, Yamane T, Lebl DR, Swijnenburg RJ, Chang CP, Quertermous T, Robbins RC.  J Heart Lung Transplant.  2005; 24 (6): 737-44
• Calcineurin is required in urinary tract mesenchyme for the development of the pyeloureteral peristaltic machinery. Chang CP,  McDill BW, Neilson JR, Joist HE, Epstein JA, Crabtree GR, Chen F.  J Clin Invest.  2004; 113 (7): 1051-8
• Injectable bioartificial myocardial tissue for large-scale intramural cell transfer and functional recovery of injured heart muscle. Kofidis T,  de Bruin JL, Hoyt G, Lebl DR, Tanaka M, Yamane T, Chang CP, Robbins RC.  J Thorac Cardiovasc Surg.  2004; 128 (4): 571-8
• Sonographic staging of the developmental status of mouse embryos in utero. Chang CP,  Chen L, Crabtree GR.  Genesis.  2003; 36 (1): 7-11
• Clinical use of cardiac ultrasound performed with a hand-carried device in patients admitted for acute cardiac care. Rugolotto M,  Chang CP, Hu B, Schnittger I, Liang DH.  Am J Cardiol.  2002; 90 (9): 1040-2
• Alternative approach for use of a left ventricular assist device with a thrombosed prosthetic valve. Pelletier MP,  Chang CP, Vagelos R, Robbins RC.  J Heart Lung Transplant.  2002; 21 (3): 402-4
• Chimeric oncoprotein E2a-Pbx1 induces apoptosis of hematopoietic cells by a p53-independent mechanism that is suppressed by Bcl-2. Smith KS,  Jacobs Y, Chang CP, Cleary ML.  Oncogene.  1997; 14 (24): 2917-26
• The Hox cooperativity motif of the chimeric oncoprotein E2a-Pbx1 is necessary and sufficient for oncogenesis. Chang CP,  de Vivo I, Cleary ML.  Mol Cell Biol.  1997; 17 (1): 81-8
• Hox homeodomain proteins exhibit selective complex stabilities with Pbx and DNA. Shen WF,  Chang CP, Rozenfeld S, Sauvageau G, Humphries RK, Lu M, Lawrence HJ, Cleary ML, Largman C.  Nucleic Acids Res.  1996; 24 (5): 898-906
• Pbx modulation of Hox homeodomain amino-terminal arms establishes different DNA-binding specificities across the Hox locus. Chang CP,  Brocchieri L, Shen WF, Largman C, Cleary ML.  Mol Cell Biol.  1996; 16 (4): 1734-45
• The mechanism of V(D)J recombination: site-specificity, reaction fidelity and immunologic diversity. Lieber MR,  Chang CP, Gallo M, Gauss G, Gerstein R, Islas A.  Semin Immunol.  1994; 6 (3): 143-53