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Seunghee Cha, D.D.S., Ph.D.

Seunghee Cha

Department of Oral & Maxillofacial Diagnostic Sciences

Section of Oral Medicine, Associate Professor
Oral Biology, Joint Associate Professor

Phone: 352-273-6687
Fax: 352-846-0588
E-mail: scha@dental.ufl.edu
P.O. Box 100414
Gainesville, FL 32610-0416

Education

  • Ph.D., University of Florida, Immunology/Microbiology, 2001
  • D.D.S., Yonsei University, Seoul, Korea, 1993

Research Interests

  • Sjӧgren’s syndrome
  • Autoimmunity/autoantibodies
  • Salivary gland regeneration/Stem cells
  • miRNA in innate immunity

Main Interests

Sjögren’s syndrome (SjS) is an autoimmune disorder that attacks the exocrine lacrimal and salivary glands, resulting in dry eyes and dry mouth, respectively. Our main research goals are to understand the pathogenesis of SjS using the various tools of molecular biology and immunology and develop strategies to alleviate dry mouth caused by SjS or radiation therapy for head and neck cancer. Our current work focuses on the identification of miRNA functions in innate immunity of SjS and the pathological roles of autoantibodies targeting muscarinic type-3 receptor (M3R). In addition, transcription factors that drive bone marrow-derived mesenchymal stem cells into salivary epithelial precursors are being investigated for future clinical translational studies. My lab utilizes in vitro cell culture system (expression vectors and mutation constructs), mouse models (disease models, knock-outs, and transgenic mice), and human specimens from patients with autoimmune conditions for current research projects.

Current and future studies include:

  • Investigation of pathological roles of anti-M3R autoantibodies in SjS hyposalivation
  • Investigation of pro-inflammatory microenvironment in the salivary glands for target tissue specificity
  • microRNA expression and their functions in innate immunity of SjS
  • Identification of susceptibility genes by applying functional genomics and proteomics
  • Application of receptor mediated siRNA delivery in SjS
  • Development of preventive and therapeutic strategies for dry mouth: proteomics/stem cell research

Selected Publications

  • Park YJ, Koh J, Kwon J, Chen S, and Cha S. (2014). “Identification of regulatory factors for BM-MSC   differentiation into salivary epithelial precursors in a co-culture system”. PLoS One. 17;9(11):e112158.
  • Pauley KM and Cha S (2013). “RNAi Therapeutics in Autoimmune Disease”, Pharmaceuticals. 6(3):287-294.
  • Lee BH, Gauna AE, Perez G, Park YJ, Pauley KM, Kawai T, Cha S. (2013). “Autoantibodies against muscarinic type 3 receptor in Sjögren’s Syndrome inhibit aquaporin 5 trafficking.”, PLoS One, 8(1):e53113.
  • Lee BH, Gauna AE, Pauley KM, Park YJ, and Cha S. (2012). “Animal models in autoimmune diseases: Lessons learned from mouse models for Sjögren’s Syndrome”, Clinical Reviews in Allergy and Immunology, 42(1):35-44.
  • Pauley MK, Stewart C, Dupre L, Kuklani R, Chan AL, Pauley BA, Reeves WH, Chan EKL, and Cha S. (2011). “Altered miR-146a expression in Sjögren’s syndrome and its functions in innate immunity”, European Journal of Immunology, 41(7):2029-39.
  • Pauley MK, Gauna EA, Grichtchenko II, Chan EKL, and Cha S, (2011). “A secretagogue-siRNA conjugate confers resistance to cytotoxicity in an in vitro model of Sjögren’s syndrome”, Arthritis and Rheumatism, 63(10): 3116-25
  • Chuong C, Pauley MK, Katz J, Bulosan M, and Cha S. (2009). “RAGE expression and NF-κB activation attenuated by extracellular domain of RAGE in human salivary gland cell line”, Journal of Cellular Physiology 221(2):430-4.
  • Pauley KM, Cha S, and Chan EKL. (2009). “miRNA in autoimmunity and autoimmune diseases”, Journal of Autoimmunity, 32 (3-4):189-94.
  • Bulosan M, Pauley K, Yo K, Chan E, Katz J, Peck A, and Cha (2009). “Inflammatory caspases are critical for enhanced cell death in the target tissue of Sjögren’s syndrome prior to disease onset.” Immunology and Cell Biology, 87(1):81-90.
  • Nguyen C, Cha S, and Peck AB. (2007). “Sjögren’s syndrome (SjS)-like disease of mice: the importance of B lymphocytes and autoantibodies.” Frontiers in Bioscience. 1(12):1767-89.
  • Nguyen C., Singson E., Kim J-Y., Cornelius J.G., Attia R., Doyle M.E., Bulosan M., Cha S. & Peck A.B. (2006). “Sjögren’s syndrome-like disease of C57BL/6.NOD-Aec1Aec2 mice: Gender differences in keratoconjunctivitis sicca defined by a cross-over in the chromosome 3 Aec1 locus.” Scand. J. Immunology. 64(3):295-307.
  • Cha S., Singson E., Cornellius J., Jarajapu Y., Knot H., and Peck AB. (2006). Muscarinic acetylcholine type-3 receptor desensitization due to chronic exposure to Sjögren’s Syndrome-associated autoantibodies. Journal of Rheumatology. 33(2):296-306.
  • Gao J., Killedar S., Cornelius J., Nguyen C., Cha, S., and Peck AB. (2006). Impact of the cytokine IL-4 on the clinical course of Sjögren’s syndrome- like disease in the NOD mouse model. Journal of Autoimmunity. 26(2):90-103.
  • Nguyen C., Singson E., Cornelius J., Killedar S., Cha. S., and Peck AB. (2006). Role of complement and B cells in Sjögren’s syndrome- like autoimmune exocrinopathy in the NOD.B10.H2 b mouse model. Molecular Immunology. 43(9):1332-9.
  • Cha, S., Brayer, J., Gao, J., Brown, V., Killedar, S., Yasunari, U., & Peck, A.B. (2004). A dual role for interferon-gamma in the pathogenesis of Sjögren’s syndrome-like autoimmune exocrinopathy in the nonobese diabetic mouse. Scand J Immunol, 60(6), 552-65.
  • Gao, J., Cha, S., Jonsson, R., Opalko, J., & Peck, A.B. (2004). Detection of anti-type 3 muscarinic acetylcholine receptor autoantibodies in the sera of Sjögren’s syndrome patients by use of a transfected cell line assay. Arthritis Rheum, 50(8), 2615-21.
  • Cha, S., Nagashima, H., Brown, V.B., Peck, A.B., & Humphreys-Beher, M.G. (2002). Two NOD Idd-associated intervals contribute synergistically to the development of autoimmune exocrinopathy (Sjögren’s syndrome) on a healthy murine background. Arthritis Rheum, 46(5), 1390-8.
  • Bulosan M., Pauley K., Yo K, Chan E, Katz J, Peck A, and Cha S. 2008 Inflammatory caspases are critical for enhanced cell death in the target tissue of Sjögren’s syndrome prior to disease onset. Immunology and Cell Biology, Submitted.
  • Stewart, C, Cha S., Bhattacharyya, I., Bulosan, M., Berg, K., Peck, AB., and Katz J. 2008 “Relationship between apoptosis and IL-4 receptor in Sjögren’s syndrome salivary glands: findings from a preliminary study.” Scandinavian journal of Rheumatology, Submitted
  • Stewart C., Cha S., Bhattacharyya I., Berg K., and Reeves W. 2008. “Salivary gland dysfunction and quality of life in Sjögren’s syndrome : A critical oral-systemic connection”, Journal of American Dental Association, 139(3):291-9.
  • Stewart C., Cha S., Caudle R., Berg K., and Katz J. 2008 “Decreased levels of soluble receptor for advanced glycation end products (sRAGE) in patients with primary Sjögren’s syndrome”, Rheumatology International, 2008 Jun;28(8):771-6.
  • Stewart C., Bhattacharyya I., Nair M., Pettigrew J., Cha S., and Katz J. “Salivary gland disorders”, Book Chapter In Oral Medicine, Radiology and Pathology, Elselvier Publisher, In Press.
  • Nguyen C, Cha S, and Peck AB. 2007. “Sjögren’s syndrome (SjS)-like disease of mice: the importance of B lymphocytes and autoantibodies.” Frontiers in Bioscience. 1(12):1767-89.
  • Nguyen C., Singson E., Kim J-Y., Cornelius J.G., Attia R., Doyle M.E., Bulosan M., Cha S. & Peck A.B. 2006. “Sjögren’s syndrome-like disease of C57BL/6.NOD-Aec1Aec2 mice: Gender differences in keratoconjunctivitis sicca defined by a cross-over in the chromosome 3 Aec1 locus.” Scand. J. Immunology. 64(3):295-307.
  • Cha S., Singson E., Cornellius J., Jarajapu Y., Knot H., and Peck AB. (2006). Muscarinic acetylcholine type-3 receptor desensitization due to chronic exposure to Sjögren’s Syndrome-associated autoantibodies. Journal of Rheumatology. 33(2):296-306.
  • Gao J., Killedar S., Cornelius J., Nguyen C., Cha, S., and Peck AB. (2006). Impact of the cytokine IL-4 on the clinical course of Sjögren’s syndrome- like disease in the NOD mouse model. Journal of Autoimmunity. 26(2):90-103.
  • Nguyen C., Singson E., Cornelius J., Killedar S., Cha. S., and Peck AB. (2006). Role of complement and B cells in Sjögren’s syndrome- like autoimmune exocrinopathy in the NOD.B10.H2 b mouse model. Molecular Immunology. 43(9):1332-9.
  • Cha, S., Brayer, J., Gao, J., Brown, V., Killedar, S., Yasunari, U., & Peck, A.B. (2004). A dual role for interferon-gamma in the pathogenesis of Sjögren’s syndrome-like autoimmune exocrinopathy in the nonobese diabetic mouse. Scand J Immunol, 60(6), 552-65.
  • Gao, J., Cha, S., Jonsson, R., Opalko, J., & Peck, A.B. (2004). Detection of anti-type 3 muscarinic acetylcholine receptor autoantibodies in the sera of Sjögren’s syndrome patients by use of a transfected cell line assay. Arthritis Rheum, 50(8), 2615-21.
  • Cha, S., Nagashima, H., Peck, A.B., & Humphreys-Beher, M.G. (2002). IDD3 and IDD5 alleles from nod mice mediate Sjögren’s syndrome-like autoimmunity. Adv Exp Med Biol, 506(Pt B), 1035-9.
  • Cha, S., Nagashima, H., Brown, V.B., Peck, A.B., & Humphreys-Beher, M.G. (2002). Two NOD Idd-associated intervals contribute synergistically to the development of autoimmune exocrinopathy (Sjögren’s syndrome) on a healthy murine background. Arthritis Rheum, 46(5), 1390-8.
  • Cha, S., Peck, A.B., & Humphreys-Beher, M.G. (2002). Progress in understanding autoimmune exocrinopathy using the non-obese diabetic mouse: an update. Crit Rev Oral Biol Med, 13(1), 5-16.