Researcher Profile

Researcher Profile

Ian Zagon, MS, PhD

Ian Zagon, MS, PhD

Distinguished Professor, Department of Neural and Behavioral Sciences
Scientific Program:Experimental Therapeutics
isz1@psu.edu

Research Interests

The laboratory of Dr. Ian Zagon investigates a novel regulatory pathway, present in a variety of cells and tissues that comprises an endogenous opioid peptide termed opioid growth factor (OGF) and its receptor, OGFr. OGF is an inhibitory growth factor that maintains homeostatic function of cell replication by binding to OGFr, a nuclear-associated receptor. The OGFr gene has been cloned in the Zagon lab, and the human chromosomal location is 20q13.3. OGF binds to OGFr, is transported into the nucleus, upregulates cyclin-dependent inhibitory kinases and subsequently down-regulates the cell cycle.

Currently, the lab’s work is a combination of basic and translational studies focusing on different disease states (i.e., cancer, autoimmune disorders and diabetic complications). Of current interest is the hypothesis that OGF levels are low in autoimmune disorders. Hence, low doses of naltrexone (LDN) that stimulate endogenous OGF production or exogenous OGF treatments are effective at inhibiting inflammatory cell proliferation, thus reversing behavioral deficits and reducing pain. Clinical and animal studies are being used to investigate the role of LDN as a treatment of autoimmune disorders (e.g., Crohn’s, fibromyalgia and multiple sclerosis).

In addition to pursuing the basic biology of the OGF-OGFr axis, the lab is interested in the repercussions of overexpression of OGF and the resulting depressed cell replication often manifested as delayed epithelialization of the cornea following abrasion, dry eye disease, ocular surface hypersensitivity and/or delayed healing of full-thickness cutaneous wounds leading to diabetic foot ulcers. Continuous or total blockade of the OGF-OGFr axis with novel therapeutics has resulted in a reversal of these complications in type 1 diabetic rats, type 2 diabetic mice, and normal animals with specific defects.

Modulation of the OGF-OGFr pathway with receptor antagonists has resulted in a number of therapies that have been patented; several start-up companies have been formed and IP licensed for further commercialization.

  • Opioid Analgesics
  • Intercellular Signaling Peptides and Proteins
  • Naltrexone
  • methionine-enkephalin receptor
  • Growth
  • Brain
  • Neoplasms
  • Opioid Receptors
  • Enkephalins
  • Therapeutics
  • Cell Proliferation
  • Narcotic Antagonists

Recent Publications

2019

Titunick, MB, Lewis, G, Cain, J, Zagon, I & McLaughlin, P 2019, 'Blockade of the OGF-OGFr pathway in diabetic bone' Connective Tissue Research. https://doi.org/10.1080/03008207.2019.1593396
McLaughlin, P, Sassani, J, Titunick, MB & Zagon, I 2019, 'Efficacy and safety of a novel naltrexone treatment for dry eye in type 1 diabetes' BMC Ophthalmology, vol. 19, no. 1, 35. https://doi.org/10.1186/s12886-019-1044-y

2018

Zagon, I & McLaughlin, P 2018, 'Intermittent blockade of OGFr and treatment of autoimmune disorders', Experimental Biology and Medicine, vol. 243, no. 17-18, pp. 1323-1330. https://doi.org/10.1177/1535370218817746

2017

Ludwig, MD, Zagon, I & McLaughlin, P 2017, 'Elevated serum [Met5]-enkephalin levels correlate with improved clinical and behavioral outcomes in experimental autoimmune encephalomyelitis', Brain Research Bulletin, vol. 134, pp. 1-9. https://doi.org/10.1016/j.brainresbull.2017.06.015
McLaughlin, P, Cain, J, Titunick, MB, Sassani, J & Zagon, I 2017, 'Topical Naltrexone is a Safe and Effective Alternative to Standard Treatment of Diabetic Wounds', Advances in Wound Care, vol. 6, no. 9, pp. 279-288. https://doi.org/10.1089/wound.2016.0725

2016

Kren, NP, Zagon, I & McLaughlin, P 2016, 'Featured Article: Nuclear export of opioid growth factor receptor is CRM1 dependent', Experimental Biology and Medicine, vol. 241, no. 3, pp. 273-281. https://doi.org/10.1177/1535370215605585
Hammer, LA, Waldner, H, Zagon, I & McLaughlin, P 2016, 'Opioid growth factor and low-dose naltrexone impair central nervous system infiltration by CD4 + T lymphocytes in established experimental autoimmune encephalomyelitis, a model of multiple sclerosis', Experimental Biology and Medicine, vol. 241, no. 1, pp. 71-78. https://doi.org/10.1177/1535370215596384
Sassani, J, Mc Laughlin, PJ & Zagon, I 2016, 'The Yin and Yang of the Opioid Growth Regulatory System: Focus on Diabetes - The Lorenz E. Zimmerman Tribute Lecture', Journal of Diabetes Research, vol. 2016, 9703729. https://doi.org/10.1155/2016/9703729
Liang, D, Sassani, J, McLaughlin, P & Zagon, I 2016, 'Topical Application of Naltrexone to the Ocular Surface of Healthy Volunteers: A Tolerability Study', Journal of Ocular Pharmacology and Therapeutics, vol. 32, no. 2, pp. 127-132. https://doi.org/10.1089/jop.2015.0070

2015

McLaughlin, P & Zagon, I 2015, 'Duration of opioid receptor blockade determines biotherapeutic response' Biochemical Pharmacology, vol. 97, no. 3, pp. 236-246. https://doi.org/10.1016/j.bcp.2015.06.016
McLaughlin, P, McHugh, DP, Magister, MJ & Zagon, I 2015, 'Endogenous opioid inhibition of proliferation of T and B cell subpopulations in response to immunization for experimental autoimmune encephalomyelitis' BMC Immunology, vol. 16, no. 1, 24. https://doi.org/10.1186/s12865-015-0093-0
Hammer, LA, Zagon, I & McLaughlin, P 2015, 'Improved clinical behavior of established relapsing-remitting experimental autoimmune encephalomyelitis following treatment with endogenous opioids: Implications for the treatment of multiple sclerosis' Brain Research Bulletin, vol. 112, pp. 42-51. https://doi.org/10.1016/j.brainresbull.2015.01.009
Turel, AP, Oh, KH, Zagon, I & McLaughlin, P 2015, 'Low Dose Naltrexone for Treatment of Multiple Sclerosis: A Retrospective Chart Review of Safety and Tolerability', Journal of Clinical Psychopharmacology, vol. 35, no. 5, pp. 609-611. https://doi.org/10.1097/JCP.0000000000000373
Kren, NP, Zagon, I & McLaughlin, P 2015, 'Mutations in the opioid growth factor receptor in human cancers alter receptor function', International Journal of Molecular Medicine, vol. 36, no. 1, pp. 289-293. https://doi.org/10.3892/ijmm.2015.2221

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