Colleen Hegg, Ph.D.
- H-K, Environmental Faculty, Neuropharmacology Faculty
Associate Professor, Pharmacology & Toxicology
Dr. Colleen Hegg
B439 Life Sciences
1355 Bogue Street
East Lansing, MI 48824
Fields of Interest: The Hegg lab research is focused on adult neurogenesis and investigates (1) the role and mechanisms of signalling of various trophic factors and (2) the effects of environmental pollutants on neurogenesis.
- 1990 - B.A., Chemistry, Kalamazoo College
- 1996 - Ph.D., Environmental Toxicology, University of Wisconsin-Madison
- 1996-99 - Postdoctoral Fellow, University of Minnesota-Minneapolis
- 2000-03 - Research Associate, Physiology, University of Utah
- 2003-06 - Research Assistant Professor, Physiology, University of Utah
- 2006-2012 - Assistant Professor, Pharmacology and Toxicology, Michigan State University
- 2012-present - Associate Professor, Pharmacology and Toxicology, Michigan State University
My research program is centered around neurogenesis, and as a neurotoxicologist, I seek ways to prevent or ameliorate the adverse effects of toxicants on the nervous system. Overall, the adult nervous system has a limited capacity to undergo post-injury repair, which is why nerve injury and neurodegenerative diseases can have devastating effects. However, neuroscientists have recently discovered that some regions of the brain are able to make new neurons (undergo neurogenesis) throughout adulthood. We know that these regions of the brain are able to undergo neurogenesis because they have stem cells that can differentiate into neurons. However, we do not know what signals or growth factors activate a stem cell to turn into a neuron.
I use the olfactory epithelium in the nose, one of the regions where neurogenesis occurs continuously, to study injury-induced neuroregeneration. The stem cells in the olfactory epithelium are similar to stem cells in the central nervous system. In comparison to stem cells in the central nervous system, olfactory stem cells are numerous and are easy to obtain via a simple biopsy. In addition, substances such as growth factors that are instilled into the nose travel directly delivered to the brain. Thus, the information I gather on growth factors and mechanisms of neurogenesis in the olfactory system will also contribute to the development of therapeutics to treat brain damage and degenerative diseases such as Parkinson’s disease, spinal cord injury, amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS).
Elucidating the Mechanisms of Injury-Evoked Regeneration in the Mouse Olfactory System
The olfactory neuroepithelium (OE) is often easily damaged as it is in direct contact with airborne pollutants, toxicants, and microbes. Although the olfactory epithelium exhibits a remarkable capacity for regeneration, the signals that lead to increased cell proliferation and neurogenesis after injury are poorly understood. I have a number of projects in the lab:
Purinergics in Adult Neurogenesis
I identified that ATP is a key signal that begins the process of regeneration. I demonstrated that pharmacological agents that specifically target the purinergic receptors can regulate the process of regeneration. These results identified targets and defined conditions for neuronal restoration therapy.
Effect of Environmental Pollutants on Neurogenesis
I am investigating the effects of exposure to relevant air pollutants and airborne toxins generated by black mold on the ability to smell and generate new neurons. My research will identify preventative strategies aimed to minimize hazardous environmental exposure and identify therapeutic targets to ameliorate damage.
Neuropeptide Y in Neurogenesis
My lab is discovering critical growth factors such as neuropeptide Y that are required for neurogenesis. My results will contribute to the development of therapeutics to enhance recovery and restore function in the olfactory system and to repair and regenerate the CNS following injury or disease.
Olfactory dysfunction, prevalent in the elderly, leads to a decrease in an individual’s health and quality of life. An age-related decline in olfaction may be related to a decrease in specific cells that release signals such as ATP and neuropeptide Y that initiate neurogenesis. Understanding these signaling pathways and how they alter with age will help us identify the cause of age-related decline in smell, and may identify therapeutic targets for prevention and treatment of olfactory dysfunction.
Cannabinoids in Adult Neurogenesis
Cannabinoids are a family of compounds involved in neurogenesis and are most widely known for causing the psychoactive effects of Cannabis (marijuana). However, cannabinoids also regulate appetite and pain-sensation, for which they are increasingly being used therapeutically in the elderly. My research will provide a detailed understanding of the chronic effects of cannabinoids on neurogenesis in adolescence and the elderly. Through both recreational and therapeutic use, chronic exposure to cannabinoids is prevalent in these age groups. My research will aid in the development and utilization of cannabinoids as appropriate pharmaceutics and/or prophylactic therapies for the treatment of chronic diseases and addiction intervention treatment.
- Shih-Chun Wang New Investigator Award, American Physiological Society, 2008
- New Investigator Award, CNS Section, American Physiological Society, 2007
Memberships in Professional Societies
- American Physiological Society
- American Society for Pharmacology and Experimental Therapeutics
- Association for Chemoreception Sciences
- Society for Neuroscience
Committees: [Michigan State University]
College of Veterinary Medicine
- Chair, Curriculum Committee, College of Veterinary Medicine, 2010-2012; Secretary, 2009-2010
- Co-Chair, Judging, College of Veterinary Medicine Phi Zeta Research Day, 2007-2015
- Member, Scholarship Committee, College of Veterinary Medicine, 2010-2015
- Member Committee on Diversity and Affirmative Action, 2007-2009
Department of Pharmacology and Toxicology
- Member, Graduate Committee, 2009-present; 2006-2007
- Judge, Pharmacology Research Colloquium, 2010-2011
- Member, Course and Curriculum Committee, 2008-2009
- Member, Outreach Committee, 2007-present
- Member, Ad Hoc Committee to Revise Website, 2006-2007
- Member, Faculty advisory Committee, 2013-present
- Member, Graduate Affairs Committee, 2008-2011
- Member, IACUC, 2013-present
- Grant Reviewer, Intramural Research Grants Program, 2008-2010
Other Committees and Service
- Grant Reviewer, Deutsche Forschungsgemeinschaft (German Research Foundation), 2011
- Grant Reviewer, Canada Foundation for Innovation, Leaders Opportunity Fund, 2009
- Grant Reviewer, NIH (Somatosensory and Chemosensory Systems) special emphasis panel, 2009
- Review Panel, Caroline tum Suden/Francis Hellebrandt Professional Opportunity Awards, 2007-2011
- Review Panel, Bodil Schmidt-Nielsen Distinguished Mentor and Scientist Award, 2007-2009
- 2011 Election Committee, Association for Chemoreception Sciences
- 2007-2009 Mentor, MentorNet, E-mentoring Network for Diversity in Engineering and Science
- 2007-2009 Women in Physiology Committee, American Physiological Society
- 2007-2009 CNS Section Steering Committee, American Physiological Society
- 2005-2008 Finance Committee, Association for Chemoreception Sciences
Full list of publications at MSU Scholars
- Jia C, Hayoz S, Hutch CR, Iqbal TR, Pooley AE, Hegg CC. An IP3R3- and NPY-expressing microvillous cell mediates tissue homeostasis and regeneration in the mouse olfactory epithelium. PLoS One. 2013;8(3):e58668. doi: 10.1371/journal.pone.0058668. Epub 2013 Mar 13. PubMed PMID: 23516531; PubMed Central PMCID: PMC3596314.
- Hayoz S, Jia C, Hegg C. Mechanisms of constitutive and ATP-evoked ATP release in neonatal mouse olfactory epithelium. BMC Neurosci. 2012 May 28;13:53. doi:10.1186/1471-2202-13-53. PubMed PMID: 22640172; PubMed Central PMCID: PMC3444318.
- Jia C, Hegg CC. Neuropeptide Y and extracellular signal-regulated kinase mediate injury-induced neuroregeneration in mouse olfactory epithelium. Mol Cell Neurosci. 2012 Feb;49(2):158-70. doi: 10.1016/j.mcn.2011.11.004. Epub 2011 Nov 30. PubMed PMID: 22154958; PubMed Central PMCID: PMC3278505.
- Jia C, Sangsiri S, Belock B, Iqbal TR, Pestka JJ, Hegg CC. ATP mediates neuroprotective and neuroproliferative effects in mouse olfactory epitheliumfollowing exposure to satratoxin G in vitro and in vivo. Toxicol Sci. 2011 Nov;124(1):169-78. doi: 10.1093/toxsci/kfr213. Epub 2011 Aug 24. PubMed PMID: 21865290; PubMed Central PMCID: PMC3196654.
- Jia C, Cussen AR, Hegg CC. ATP differentially upregulates fibroblast growth factor 2 and transforming growth factor α in neonatal and adult mice: effect on neuroproliferation. Neuroscience. 2011 Mar 17;177:335-46. doi: 10.1016/j.neuroscience.2010.12.039. Epub 2010 Dec 25. PubMed PMID: 21187124; PubMed Central PMCID: PMC3049987.