Associate Professor of Research Surgery, Keck School of Medicine of USC
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Education

Medical School: 

University of Oklahoma, Norman, Oklahoma, M.S., 1980, University of Oklahoma, Norman, Oklahoma, Ph.D., 1984, University of Texas Southwestern Medical Center at Dallas, Texas, Postdoctoral Training, 1984-1988 (Mentor: Fred Grinnell)

Publications: 

T.-L. Tuan, A. K. Song, S. Chang, S. Younai, and M.E. Nimni. In vitro fibroplasia: Matrix contraction, cell growth and collagen production of fibroblasts cultured in 3-dirnensional fibrin matrix. Exp. Cell Res., 223: 127-134, 1996. (PMID: 8635484)


WY Li, EY Huang, M. Dudas, D. Warburton, V. Kaartinen, T.-L. Tuan. Transforming growth factor-beta3 affects plasminogen activator inhibitor-1 expression in fetal mice and modulates fibroblast-mediated collagen gel contraction. Wound Repair Regeneration. 2006 Sep-Oct;14(5):516-25.

T.-L. Tuan, P. Hwu, W. Ho, P. Yiu, R. Chang, A. Wysocki, P. D. Benya. Adenoviral overexpression and siRNA suppression demonstrate that plasminogen activator inhibitor-1 produces elevated collagen accumulation in normal and keloid fibroblasts. Am. J. Pathology, 173:1311-1325, 2008. (PMID: 18832570)

YS. Lee, A. Wysocki, D. Warburton, T.-L. Tuan. Wound healing in development. Birth Defects Res C Embryo Today. 2012 Sep;96(3):213-22. Review. (peer reviewed) (PMID: 23109317).

Lee YS, Hsu T, Chiu WC, Sarkozy H, Kulber DA, Choi A, Kim EW, Benya PD, Tuan TL. (2015) Keloid-derived, plasma/fibrin-based skin equivalents generate de novo dermal and epidermal pathology of keloid fibrosis in a mouse model. Wound Repair Regen. 2016 Mar;24(2):302-16. doi: 10.1111/wrr.12397.PMID: 26683740

Research Interests: 

General: Extracellular Matrix Modulation of Cellular Gene Expressions

Specific: Keloid Pathogenesis; Keloid Animal Model and Therpeutic Intervention, Molecular Mechanisms in Cell and Extracellular Matrix Interactions during Tissue Repair: Integrin Functions, Growth Factor Modulations, Protease/Inhibitor Expressions, and Extracellular Matrix Remodeling, Epithelial-Mesenchyme Interactions during Tissue Repair/Regeneration, Fetal Scarless Skin Wound Repair, In Vitro Tissue Equivalents: Three Dimensional Matrix Culture Model Systems, Healing of Problematic Wounds: Hypertrophic Scars, Keloids, and Chronic Wounds

RESEARCH FOCUS

Dr. Tuan received her postdoctoral training in the area of Cell-ECM interactions from Dr. Fred Grinnell at the University of Texas Southwestern Medical Center at Dallas. The in vitro three dimensional fibrin matrix model of fibroplasia for wound healing was established in the early stage of her independent research career. Using the model system and in collaboration closely with her clinical and other colleagues, the molecular phenotype of keloid fibroblasts to include plasminogen activator inhibitor-1 (PAI-1) was discovered with evidence supporting the role PAI-1 in collagen accumulation (Am J. Pathol., 173(5):1311-25, 2008). Extending from the experience and established work, Dr. Tuan has taken a focused effort in the past several years to generate a clinically relevant and deliverable keloid-derived, plasma/fibrin-based skin equivalent animal model of keloid fibrosis that bridges the major gap of keloid translational research (Wound Repair Regen., 24(2):302-16, 2016). The model epitomizes the injury-repair environment in triggering and fostering keloid formation and the dynamic epidermal/dermal interactions which occur during disease development. The biological continuity of keloid genesis in the model system provides an accessible platform to elucidate the disease mechanism and test knowledge-based therapies. Dr. Tuan’s research has been supported by the National Institutes of Health (NIH), Department of Health and Human Services, USA.

KEY FINDINGS

1. In vitro fibroplasia - the three dimensional fibrin matrix culture system for wound healing.

2. Developmental differences in the expression and modulation of extracellular matrix proteases and inhibitors in mouse fetal skin and skin wounds

3. Adenoviral overexpression and small interfering RNA suppression demonstrate that plasminogen activator inhibitor-1 produces elevated collagen accumulation in normal and keloid fibroblasts.

4. Keloid-derived, plasma/fibrin-based skin equivalents generate de novo dermal and epidermal pathology of keloid fibrosis in a mouse model.

CURRENT RESEARCH STUDIES

Keloid-derived, Plasma/Fibrin-Based Skin Equivalents Generate De Novo Dermal and Epidermal Pathology of Keloid Fibrosis in a Mouse Model

CURRENT FUNDINGS

1 R01 GM095821-01 Tuan & Benya (Co-PIs)

4/01/2012-2/28/2017 "siRNA Inhibition of Keloid Fibrosis in Fibrin Matrix Skin Equivalent Mouse Models"

Total Cost: $1,200,000

Sanovi-Gazyme Tuan (PI)

05/01/2016-10-31-2016 “Keloid Therapeutic: Targetig PAI-1”

Total Cost: $100,000

 

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