ArticleNature communications2023
Role of TMEM100 in mechanically insensitive nociceptor un-silencing.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Ultraviolet-B sensitizes silent nociceptors and desensitizes C-touch fibers to slow depolarizing electrical stimuli in pigs.Pain reports · 2026Article
- Perifollicular stromal cells sustain folliculogenesis via MDK-NCL signaling in mice and humans.Cell discovery · 2026Article
- CHRNA3⁺ nociceptors prime the cutaneous sensory interface to enhance electroacupuncture analgesia.Chinese medicine · 2026Article
- Tooth Pulp Afferents and Transient Receptor Potential (TRP) Ion Channels as Key Regulators of Pulp Homeostasis, Inflammation, and Pain.International journal of molecular sciences · 2025Review
- Article
- Enkephalin-producing regulatory T cells in the skin restrain local inflammation through control of nociception.Science immunology · 2025Article
- The activation thresholds and inactivation kinetics of poking-evoked PIEZO1 and PIEZO2 currents are sensitive to subtle variations in mechanical stimulation parameters.Channels (Austin, Tex.) · 2024Article
- PIEZO ion channels: force sensors of the interoceptive nervous system.The Journal of physiology · 2024Review
Corrections and comments
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Authors and funding
18 authors at 7 institutions in 5 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanically silent nociceptors are sensory afferents that are insensitive to noxious mechanical stimuli under normal conditions but become sensitized to such stimuli during inflammation. Using RNA-sequencing and quantitative RT-PCR we demonstrate that inflammation upregulates the expression of the transmembrane protein TMEM100 in silent nociceptors and electrophysiology revealed that over-expression of TMEM100 is required and sufficient to un-silence silent nociceptors in mice. Moreover, we show that mice lacking TMEM100 do not develop secondary mechanical hypersensitivity-i.e., pain hypersensitivity that spreads beyond the site of inflammation-during knee joint inflammation and that AAV-mediated overexpression of TMEM100 in articular afferents in the absence of inflammation is sufficient to induce mechanical hypersensitivity in remote skin regions without causing knee joint pain. Thus, our work identifies TMEM100 as a key regulator of silent nociceptor un-silencing and reveals a physiological role for this hitherto enigmatic afferent subclass in triggering spatially remote secondary mechanical hypersensitivity during inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.