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Associate Professor, UC Department of Pediatrics
My areas of research include neuroscience, pain research and sensory neuron biology.
Our lab is investigating the mechanisms of sensory neuron sensitization with a particular emphasis on nociceptive processing. We seek to understand pain processing better to develop proper treatments.
Pain is a significant health issue that affects a large number of people worldwide. The mechanisms by which pain develops in children may be distinct from adults and influenced by non-neuronal communication. While we know a great deal of information about the role of nociceptors in the development of pain states, we do not have a comprehensive understanding of how distinct subtypes of sensory fibers modulate pain across the lifespan under different injury conditions.
Some of our discoveries include finding that peripheral growth hormone (GH) signaling to neurons not only modulates normal sensory development, but exogenous GH may also be used as a potential therapy for pediatric pain. We have obtained a U.S. patent to develop this technology. We also found that distinct growth factor signaling pathways have the ability to modulate both muscle pain and cardiovascular reflexes after ischemic injury to the periphery.
I am the recipient of numerous awards from the National Institutes of Health (NIH) that support my research that began as early as my pre-doctoral training (2006). I am also a Rita Allen Foundation Scholar (2012) and was named a Cincinnati Children's Trustee Scholar in 2013. I am an associate editor for the journals Pain and Molecular Pain and a reviewer for more than 30 other peer-reviewed journals. I have been a researcher for more than 20 years and began my work at Cincinnati Children's in 2011.
My accomplishments, awards and recognitions include:
I’m a member of the Society for Neuroscience, the US Association for the Study of Pain, the International Association for the Study of Pain and the Special Interest Group on Pain in Childhood.
Neuroscience; pain research; sensory neuron biology
Anesthesia, Neuromuscular Development
Michael P. Jankowski, PhD8/14/2020
MS: Neuroscience, University of Pittsburgh, Pittsburgh, PA, 2003.
PhD: Neurobiology, University of Pittsburgh, Pittsburgh, PA, 2006.
Postdoctoral Training: University of Pittsburgh, Pittsburgh, PA, 2006-2010.
Integrated analysis of the molecular pathogenesis of FDXR-associated disease.
Slone, JD; Yang, L; Peng, Y; Queme, LF; Harris, B; Rizzo, SJ S; Green, T; Ryan, JL; Jankowski, MP; Reinholdt, LG; et al.
Cell Death and Disease.
A dual role for peripheral GDNF signaling in nociception and cardiovascular reflexes in the mouse.
Queme, LF; Weyler, AA; Cohen, ER; Hudgins, RC; Jankowski, MP.
Proceedings of the National Academy of Sciences of USA.
Systemic growth hormone deficiency causes mechanical and thermal hypersensitivity during early postnatal development.
Ford, ZK; Dourson, AJ; Liu, X; Lu, P; Green, KJ; Hudgins, RC; Jankowski, MP.
A histone deacetylase 3-dependent pathway delimits peripheral myelin growth and functional regeneration.
He, X; Zhang, L; Queme, LF; Liu, X; Lu, A; Waclaw, RR; Dong, X; Zhou, W; Kidd, G; Yoon, S; et al.
Interleukin 1 beta inhibition contributes to the antinociceptive effects of voluntary exercise on ischemia/reperfusion-induced hypersensitivity.
Ross, JL; Queme, LF; Lamb, JE; Green, KJ; Ford, ZK; Jankowski, MP.
Systemic Delivery of AAV-Fdxr Mitigates the Phenotypes of Mitochondrial Disorders in Fdxr Mutant Mice.
Yang, L; Slone, J; Zou, W; Queme, LF; Jankowski, MP; Yin, F; Huang, T.
Molecular Therapy-Methods & Clinical Development.
Systemic administration of AAV-Slc25a46 mitigates mitochondrial neuropathy in Slc25a46-/- mice.
Yang, L; Slone, J; Li, Z; Lou, X; Hu, Y; Queme, LF; Jankowski, MP; Huang, T.
Human Molecular Genetics.
Sex differences and mechanisms of muscle pain.
Queme, LF; Jankowski, MP.
Single-cell q-PCR derived expression profiles of identified sensory neurons.
Adelman, PC; Baumbauer, KM; Friedman, R; Shah, M; Wright, M; Young, E; Jankowski, MP; Albers, KM; Koerber, HR.
The evolution and multi-molecular properties of NF1 cutaneous neurofibromas originating from C-fiber sensory endings and terminal Schwann cells at normal sites of sensory terminations in the skin.
Rice, FL; Houk, G; Wymer, JP; Gosline, SJ C; Guinney, J; Wu, J; Ratner, N; Jankowski, MP; La Rosa, S; Dockum, M; et al.