Semaphorin 4C Plexin-B2 signaling in peripheral sensory neurons is pronociceptive in a model of inflammatory pain

Eszter Paldy, Manuela Simonetti, Thomas Worzfeld, Kiran Kumar Bali, Lucas Vicuña, Stefan Offermanns and Rohini Kuner ()
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Eszter Paldy: Heidelberg University
Manuela Simonetti: Heidelberg University
Thomas Worzfeld: Marburg University
Kiran Kumar Bali: Heidelberg University
Lucas Vicuña: Heidelberg University
Stefan Offermanns: Max-Planck-Institute for Heart and Lung Research
Rohini Kuner: Heidelberg University

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Semaphorins and their transmembrane receptors, Plexins, are key regulators of axon guidance and development of neuronal connectivity. B-type Plexins respond to Class IV semaphorins and mediate a variety of developmental functions. Here we report that the expression of Plexin-B2 and its high-affinity ligand, Sema4C, persists in peripheral sensory neurons in adult life and is markedly increased in states of persistent pain in mice. Genetic deletion of Sema4C as well as adult-onset loss of Plexin-B2 leads to impairment of the development and duration of inflammatory hypersensitivity. Remarkably, unlike the neurodevelopmental functions of Plexin-B2 that solely rely on Ras signaling, we obtained genetic and pharmacological evidence for a requirement of RhoA-ROCK-dependent mechanisms as well as TRPA1 sensitization in pronociceptive functions of Sema4C-Plexin-B2 signaling in adult life. These results suggest important roles for Plexin-B2 signaling in sensory function that may be of therapeutic relevance in pathological pain.

Date: 2017
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DOI: 10.1038/s41467-017-00341-w

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