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RNA control permeates neurobiology. Nociceptors are exemplary. Noxious stimuli can
induce rapid translation in nociceptors. In prior work, we examined translational
efficiency on a genome-wide basis in DRG neurons using ribosome profiling. We found
that a single motif was highly enriched in the 3’UTRs of preferentially translated
mRNAs. It contains an A/U-rich element bound by HuR. We found that HuR is expressed
broadly throughout the PNS. To determine the role of HuR in pain, we made use of a
recently described small molecule inhibitor termed CMLD-2. It reduced spontaneous
firing of mouse and hiPSC derived sensory neurons. Furthermore, inhibition of HuR
in vivo with CMLD-2 blocks hyperalgesic priming and alleviates mechanical hypersensitivity.
Elimination of HuR from Nav1.8 expressing neurons ablates hyperalgesic priming. Collectively,
this work identifies HuR as a key factor involved in nociceptive plasticity and suggests
a new target for pain. Grant support from National Institutes of Health (NIH).
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© 2022 Published by Elsevier Inc.
