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Ching-Ling (Ellen) Lien, Ph.D.
Ching-Ling (Ellen) Lien, Ph.D.
Assistant Professor




Contact

The Saban Research Institute
Childrens Hospital Los Angeles
4650 Sunset Blvd., MS137
Los Angeles, CA 90027

Phone: (323) 361-8377
Office: SRI 422
Email: clien@chla.usc.edu

USC PIBBS Home Page
http://www.usc.edu/programs/pibbs/site/faculty/lien_c.htm

PubMed Publications
www.ncbi.nlm.nih.gov/sites/entrez?cmd=search&db=PubMed&term=%20Lien%2BCL[auth]

Education

BS 1993 - National Taiwan University
MS 1995 - National Taiwan University
PhD 2001 - University of Texas, Southwestern Medical Center, Dallas

Postdoctoral Research Fellowship

2006 Children's Hospital of Boston
Harvard Medical School

Research Description

Heart disease is among the leading causes of death for both adults and children. Mammalian hearts have very limited regenerative capacity and heal by scarring and hypertrophy after heart injury, which results in decreased cardiac performance. By contrast, zebrafish have remarkable regenerative capacity. The molecular mechanisms of zebrafish heart regeneration are not understood. The goal of my lab is to define the molecular and cellular mechanisms of heart regeneration in zebrafish with the long-term goal of enhancing regenerative capacity and replacing defective tissues in diseased human hearts.

We use genetic and genomic approaches to dissect the process of zebrafish heart regeneration. Using gene expression profiling, we identified a set of genes that are differentially expressed during heart regeneration. We would like to address the following basic questions: How do these genes contribute to heart regeneration in zebrafish? Does regeneration recapitulate the developmental process? Are stem cells also involved in this regeneration process? The functions of these genes will be characterized in cultured cardiomyocytes in vitro, zebrafish embryos and regenerating hearts in vivo.

Most zebrafish genes are highly conserved with mammalian homologues. However, zebrafish can regenerate heart but mammals can't. We would like to test the two possibilities that contribute to the incapability of regeneration: 1 mammalian hearts fail to express these genes upon injuries at the right time and place; 2. mammalian cardiomyocytes response to stimuli differently from zebrafish cardiomyocytes.

Our work may lead to discovery of important factors/pathways that can contribute to pharmaceutical or cellular therapies for ischemic or congenital heart diseases.

Selected Publications

  • Kim J, Wu Q, Zhang Y, Wiens KM, Huang Y, Rubin N, Shimada H, Handin RI, Chao MY, Tuan TL, Starnes VA and Lien CL*. PDGF signaling is required for epicardial functions and blood vessel formation in regenerating zebrafish hearts. Proc. Natl. Acad. Sci. USA 107, 17206-10.

  • Wiens KM, Lee H, Shimada H, Martin G, Metcalf AE, Chao MY, Starnes VA and Lien CL*. Platelet-derived growth factor receptor beta is critical for zebrafish intersegmental vessel formation. PLoS One 5, e11324.

  • Lien, C.-L., Schebesta, M., Makino, S., Weber, G. J. and Keating, M. T. Gene expression analysis of zebrafish heart regeneration. PLoS Biology. 4 (8) 1386-1396.

  • Schebesta M, Lien CL, Engel FB, Keating MT. Transcriptional profiling of caudal fin regeneration in zebrafish. TSW Development & Embryology 1 (S1) 38-54, 2006.

  • Whitehead, G.G., Makino, S., Lien, C.-L., and Keating, M. T. fgf20 is essential for initiating zebrafish fin regeneration. Science. (2005). 310, 1957-60.

  • Makino, S., Whitehead, G.G, Lien, C.-L., Kim, S., Jhawar, P., Kono, A. Kawata, Y. and Keating, M. T. Heat-shock protein 60 is required for blastema formation and maintenance during regeneration.  Proc. Nat. Acad. Sci. (2005). 102, 14599-604.

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