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Health Science Campus
Block Health Science Building

Mail Stop # 1007
3000 Arlington Avenue
Toledo, Ohio 43614-2598
Phone: 419.383.4109
Fax: 419.383.3008


Office: Block Health Science Building, Room 184
Tel: 419-383-4085
Lab: 419-383-4376

1991: B.A., Korea University
1998: MS, Medical University of South Carolina
2003: Ph.D., Johns Hopkins University

Research Interests:
Our first research project is to develop a new drug for the treatment of neurodegenerative diseases. Over 5 million people in the US and 35 million worldwide suffer from Alzheimer's disease (AD), a devastating disease that costs the US over $100 billion every year. Enormous efforts have been poured on the development of therapeutic agent(s) that can slow AD while current treatments only address symptoms without disease-modifying effect and have side effects. Conversely, increasing evidence points to the effectiveness of neurotrophic agents for AD treatment. However, the BBB-impermeability and short half-life of protein neurotrophic factors limit their use for AD treatment. Hence, neurotrophic agent that overcomes those shortcomings should be a better neurotrophic treatment of AD. We discovered a neuroprotrophic polysaccharide named ‘midi-GAGR’ that has good BBB-permeability, strong neuroprotective and neurotrophic effects in primary neurons and in animals, and >12-h half life. Our current research focuses on the examination of the efficacy of midi-GAGR in slowing pathogenesis in AD animals. Achieving our goal will provide a strong scientific basis for the clinical development of midi-GAGR.

Our second research project is to develop a stem cell-based treatment that can modify osteoarthritis (OA). OA is a disease caused by degradation of extracellular matrix at the cartilage of inflamed synovial joints, resulting in joint deformation and dysfunction. An estimated 27 million Americans, especially aged people, suffer from OA and the population is expected to reach 67 million in USA by 2030. Traditional OA treatments including non-steroidal anti-inflammatory drug, joint replacement, etc., have no disease-modifying effect. Given most OA treatments cannot overcome synovial inflammation that decreases cartilage formation and increases cartilage breakdown, OA-modifying treatment should suppress inflammation and increase cartilage formation. We have developed an innovative stem cell-based OA therapy device named CHAMPthat is designed to enhance cartilage formation and decrease inflammation. In our study, CHAMP could generate type II collagen-containing chondrocytes in human inflammatory OA synovial fluid while current MSC-based OA therapy could not, showing that CHAMP is superior to current MSC-based OA therapy. Given that all three CHAMP components are already used for human treatment or in clinical trial, it is expected to take a short regulatory process to obtain the approval of the use of CHAMP for human OA treatment. The current goal of our research is to examine the efficacy of CHAMP in treating OA in anterior cruciate ligament transaction (ACLT) animal model. Achieving our goal will provide solid pre-clinical and clinical bases for the clinical development of CHAMP for OA treatment.

Our third research project is to reveal the molecular mechanism that underlies the control of the directionality of vesicle movements. Hormone secretion is fundamental to the very existence of an organism, regulating important physiological functions such as neurotransmission, energy use, reproduction, and behavior, all required for the survival and maintenance of homeostasis. Understanding the mechanisms underlying how cells within the hypothalamic-pituitary axis secrete hormones is therefore of paramount importance. For example, regulated secretion of adrenocorticotropic hormone (ACTH) allows the endocrine, immune, and central nerve systems to cope with stress, while dysregulation can lead to metabolic, immune, and psychiatric disorders. Likewise, regulated secretion of the hormone oxytocin in the brain is important for controlling caloric homeostasis and social behavior, while dysregulation leads to obesity, diabetes, and psychiatric disorders such as anxiety. Nevertheless, little is known about the microtubule-based transport of vesicles containing the hormones to the secretion sites. We have discovered that A-kinase anchor protein 5 (AKAP5) is involved in the actions of protein kinase A (PKA) and protein kinase C (PKC) to control the anterograde transport of ACTH- and OXT-containing vesicles to the secretion sites in the pituitary corticotrophs and hypothalamic neurons, respectively. We found that activated PKA increases association of kinesin-2 with the AKAP5-ANXA1 complex and anterograde transport of the peptidergic vesicles while activated PKC decreases both. This evidence suggests that PKA enhances and PKC decreases the anterograde transport of the peptidergic vesicles by controlling the association of kinesin-2 with AKAP5-ANXA1 complex on the vesicles. Our goal is to identify AKAP5-mediated molecular mechanism that controls the directionality of microtubule-based transport of ACTH- and OXT-containing vesicles in the pituitary corticotrophs and hypothalamic neurons, respectively.


Academic Honors:
NICHD American Recovery and Reinvestment Act (ARRA) grant, 2009
NIH FARE (Fellows Award for Research Excellence) award, 2008
NICHD Transition Career Development K22 Award, 2007
Young Investigator Award of the Summer joint US-European Neuropeptide Conference, 2006
NIH FARE (Fellows Award for Research Excellence) award 2006
Predoctoral Fellowship NIH Training Program at Johns Hopkins University 1998-2003
Predoctoral Fellowship, EPSCOR NSF Training Program in Cell and Molecular Pharmacology

Ella, K.M., Qi, C., McNair, A.F., Park, J.H., Wisehart-Johnson, A.E., and Meier, K.E. (1997) PhospholipaseD activity in PC12 cells. Journal of Biological Chemistry, 272(20): 12909-12912.

Qi, C., Park, J.H., Shirley, D.W., Bradshaw, C.D., Ella, K.M., and Meier, K.E. (1998) Lysophosphatidic acid stimulates phospholipase D activity and cell proliferation in PC-3 human prostate cancer cells. Journal of Cellular Physiology, 174(2): 261-272.
Park,J.J., Cawley N.W., and Loh, Y.P. (2008) Carboxypeptidase E cytoplasmic tail anchors hormone vesicles to microtubule motors for transport and activity–dependent secretion. Molecular Endocrinology, 22(4): 989-1005.
Park,J.J., Cawley N.W., and Loh, Y.P. (2008) Carboxypeptidase E cytoplasmic tail anchors BDNF vesicles to microtubule motors for transport and activity – dependent secretion. Molecular and Cellular Neuroscience, 39(1): 63-73.
Park,J.J. and Loh, Y.P. (2008) How peptide hormone vesicles are transported to the secretion site for exocytosis. Molecular Endocrinology, 22(12): 2583-95.
Lou, H., Park, J.J., Sarcon, A., Adams, T., Cawley, N.X., and Loh, Y.P. (2010) Carboxypeptidase E cytoplasmic tail mediates localization of synaptic vesicles to the pre-active zone in hypothalamic nerve terminals. (co-first author) Journal of Neurochemistry, 114(3): 886-896.
Park, J.J., Gondre-Lewis, M., Kim, T., and Loh, Y.P. (2011) A distinct trans Golgi network subcompartment for sorting of synaptic and granule proteins in neuroendocrine cells. Journal of Cell Science, 124(5): 735-44.
Park,J.J. and Loh, Y.P. (2011) Visualization of peptide secretory vesicles in living nerve cells. Methods in Molecular Biology, 789:137-45.
Hensley, K., Venkova, K., Christov, A., Gunning, W., and Park, J.J. (2011) Collapsin response mediator protein-2: An emerging pathologic feature and therapeutic target for neurodisease indications. Molecular Neurobiology, 43(3): 180-91.
Cawley, N.X., Wetsel, W., Murthy, S., Park, J.J., Pacak, K., and Loh, Y.P. (2012) New roles of carboxypeptidase E in endocrine and neurological function and cancer. Endocrine Reviews, 33:216-53.
Lou, H., Park, J.J., Phillips, A., and Loh, Y.P. (2012) Gamma-adducin promotes process outgrowth and secretory protein exit from the Golgi apparatus. (co-first author) Journal of Molecular Neuroscience. 49: 1-10.
Gondre-Lewis, M., Park, J.J., and Loh, Y.P. (2012) Cellular Mechanisms for the Biogenesis  and Transport of Synaptic and Dense-Core Vesicles. (co-first author) International Review of Cell and Molecular Biology 299:27-115.
Park, J.J., Rubio, M.V., Zhang, Z., Um, T., Xie, Y., Knoepp, S.M., Snider, A.J., Gibbs, T.C., and   Meier, K.E. (2012) Effects of lysophosphatidic acid on calpain-mediated proteolysis of focal adhesion kinase in human prostate cancer cells. Prostate, 72: 1595-610.
Makani, V., Hall, J, Qamar, K., Jain, P., Hensley, K., and Park, J.J. (2013) Antidepressant inhibits microtubule organization and hormone secretion in pheochromocytoma cells. Molecular and Cellular Endocrinology, 381:175-87.
Makani V, Sultana R, Sie KS, Orjiako D, Tatangelo M, Dowling A, Cai J, Pierce W, Butterfield DA, Hill J, Park, J.J. (2013) Annexin A1 complex mediates oxytocin vesicle transport. Journal of Neuroendocrinology, 25: 1241-54.
Christopher, K., Makani, V., Judy, W., Lee, E., Chiaia, N., Kim, D.S., and and Park, J.J.  (2015) Use of fluorescent ANTS to examine the BBB-permeability of polysaccharide. MethodsX, 2: 174-181.
Makani, V., Jang, Y., Christopher, K., Judy, W., Eckstein, J., Hensley, K., Chiaia, N., Kim, D., and Park, J.J. BBB-permeable polysaccharide, midi-GAGR, has a strong neuroprotective and neurotrophic effects. Under revision for ‘PLOS ONE’.
Heck, B., Park, J.J., Makani, V., and Kim, D. PPAR-delta agonist with mesenchymal stem cells induces type II collagen-producing chondrocytes in human arthritic synovial fluid.  Under revision for ‘Cell Transplantation’.
Last Updated: 10/16/15