e-mail- fyu@med.wayne.edu

Education:
B.S., Biology, Wuhan University, Wuhan, China, 1982
Ph.D., Wayne State University, Detroit, Michigan, 1988

Professional and Faculty Appointments:
Instructor, Department of Physiology, UT Southwestern Medical Center at Dallas, Dallas, Texas, 1990-1993
Instructor, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, 1993-1998
Assistant Scientist, the Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts, 1993-2000
Assistant Professor, Department of Ophthalmology, Harvard Medical School, Boston, Massachusetts, 1999-2001
Associate Scientist, the Schepens Eye Research Institute, Harvard Medical School, Boston, Massachusetts, 2001-2001
Associate Professor, Department of Cellular Biology and Anatomy, Department of Ophthalmology, Institute of Molecular Medicine and Genetics, Medical College of Georgia, Augusta, Georgia, 2001-2004
Professor and Director of Research, the Kresge Eye Institute/ Department of Ophthalmology, Department of Anatomy and Cell Biology, Wayne State University School of Medicine, Detroit, Michigan, 2004-present

Major Research Interests:
Ocular innate immunity and corneal epithelial wound healing.

Current Research:
1) Molecular regulation of corneal wound healing.
Proper healing of corneal wounds is vital to maintaining a clear, healthy cornea and for preserving vision. Our long-term goal has been to obtain basic information about the molecular and cellular biology of corneal wound healing. Particularly critical for successful wound healing are cell migration and proliferation, processes that are driven by growth factors, such as ligands for the epidermal growth factor (EGF) receptor (EGFR), released coordinately into the injury site. Preliminary evidence suggests that ectodomain shedding of EGFR ligands such as heparin-binding EGF-like growth factor (HB-EGF), EGFR activation, and subsequent intracellular signaling are important for regulating corneal epithelial wound healing. Member(s) of the ADAM (a disintegrin and metalloprotease) family may be involved in EGFR ligand shedding. Our objective is to understand, under pathophysiological conditions, how wounding induces endogenous EGFR ligand generation and how the resulting signaling network regulates corneal epithelial cell (CEC) migration and proliferation.
2) Toll-like receptor mediated innate response of corneal epithelial cells.
The integrity of the cornea depends critically on a tightly regulated host defense apparatus. The long-term goal is to understand the role of epithelium in corneal innate immunity. Recent studies in the laboratory have shown that human corneal epithelial cells (HCECs) participate in corneal innate defense by recognizing infectious bacteria with the family of Toll-like receptors (TLRs) and by responding to infection via the expression of pro-inflammatory cytokines, chemokines, and anti-microbial molecules. The hypothesis to be tested in this application is that the epithelium, via the action of TLRs, coordinates the innate immune response to infection in the cornea. The objective is to understand the underlying mechanisms for HCECs to recognize pathogens through TLRs and to mount a protective response by releasing factors that kill pathogens and key chemokines and cytokines that prime and sensitize stromal keratocytes and direct infiltrating polymorphonuclear leukocyte in the innate defense of the cornea.
Grant Support: NIH (R01 grants), Fight for Sight, Research to Prevent Blindness (to The Department of Ophthalmology)

Recent papers:

1.	Xu KP, Ding Y, Lin J, Yu FX. Wound-induced HB-EGF ectodomain shedding and EGFR activation in corneal epithelial cell. Invest Ophthalmol Vis Sci. 45:813-820, 2004. Medline
2.	Xu KP, Zhang J, Riggs A, Yu FX. Role of ErbB2 in corneal epithelial wound healing. Invest Ophthalmol Vis Sci. 45:4277-4583, 2004. Medline
3.	Zhang J, Wu XY, and Yu FX. Inflammatory responses of corneal epithelial cells to Pseudomonas aeruginosa infection. Cur Eye Res, 30:527-34, 2005. Medline
4.	Kumar A, Zhang J, Yu F. TLR3 mediates Poly (I:C)-induced antiviral response In human corneal epithelial cells. Immunology. 117(1):11-21. 2006. Medline
5.	Kumar A, Zhang J, Yu F. Toll-like receptor 2-mediated expression of -defensin-2 in human corneal epithelial cells. Microbes and Infection. 8(2):380-9. 2006. Medline
6.	Yin J, Xu K, Zhang J, Kumar K, Yu F. Wound-induced ATP Release and Epidermal Growth Factor Receptor Activation in Epithelial Cells. J. Cell Science, 120: 815-25. 2007. Medline
7.	Xu K, Yu F. Cross-talk between c-Met and Epidermal Growth Factor Receptor during Retinal Pigment Epithelial Wound Healing. IOVS; 48: 2242-8. 2007. Medline
8.	Kumar, A., Tassopoulos, A.M., Li, Q., and Yu, F.S. Staphylococcus aureus protein A induced inflammatory response in human corneal epithelial cells. Biochem Biophys Res Commun. 354: 955-61. 2007. Medline
9.	Kumar A, Zhang J, Yin J, Yu F. Modulation of Corneal Epithelial Innate Immune Response to Pseudomonas Infection by Flagellin Pretreatment. Invest Ophthalmol Vis Sci. 48:4664-4670. Medline
10.	Kumar A, Hazlett LD, Yin J, Yu F. Flagellin Suppresses Inflammatory Response and Enhances Bacterial Clearance in Murine Model of Pseudomonas Keratitis. Infection and Immunity. 2007. Medline

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