期刊
JOURNAL OF NEUROSCIENCE
卷 41, 期 37, 页码 7712-7726出版社
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0440-21.2021
关键词
Arc; DRG; neuroinflamation; nociceptors; translational control
资金
- National Institutes of Health (NIH) [R01NS065926, R01NS098826, R01NS100788, R01NS114018]
- University of Texas STARS program
- IBRO Return Home Fellowship
- IASP Early Career Research Grant
- Cancer Prevention and Research Institute of Texas (CPRIT) Award [RP180670]
- Chan Zuckerberg Ben Barres Early Career Acceleration Award
- NIH Director's Transformative Grant [R01 NS115716]
Studies have shown that activity-dependent protein Arc plays an important role in translational regulation in sensory neurons, potentially regulating neurogenic inflammation in the skin through intercellular signaling.
Injury responses require communication between different cell types in the skin. Sensory neurons contribute to inflammation and can secrete signaling molecules that affect non-neuronal cells. Despite the pervasive role of translational regulation in nociception, the contribution of activity-dependent protein synthesis to inflammation is not well understood. To address this problem, we examined the landscape of nascent translation in murine dorsal root ganglion (DRG) neurons treated with inflammatory mediators using ribosome profiling. We identified the activity-dependent gene, Arc, as a target of translation in vitro and in vivo. Inflammatory cues promote local translation of Arc in the skin. Arc-deficient male mice display exaggerated paw temperatures and vasodilation in response to an inflammatory challenge. Since Arc has recently been shown to be released from neurons in extracellular vesicles (EVs), we hypothesized that intercellular Arc signaling regulates the inflammatory response in skin. We found that the excessive thermal responses and vasodilation observed in Arc defective mice are rescued by injection of Arc-containing EVs into the skin. Our findings suggest that activity-dependent production of Arc in afferent fibers regulates neurogenic inflammation potentially through intercellular signaling.
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