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Role of TMEM100 in mechanically insensitive nociceptor un-silencing

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Role of TMEM100 in mechanically insensitive nociceptor un-silencing. / Nees, Timo A; Wang, Na; Adamek, Pavel; Zeitzschel, Nadja; Verkest, Clement; La Porta, Carmen; Schaefer, Irina; Virnich, Julie; Balkaya, Selin; Prato, Vincenzo; Morelli, Chiara; Begay, Valerie; Lee, Young Jae; Tappe-Theodor, Anke; Lewin, Gary R; Heppenstall, Paul A; Taberner, Francisco J; Lechner, Stefan G.

In: NAT COMMUN, Vol. 14, No. 1, 05.04.2023, p. 1899.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Nees, TA, Wang, N, Adamek, P, Zeitzschel, N, Verkest, C, La Porta, C, Schaefer, I, Virnich, J, Balkaya, S, Prato, V, Morelli, C, Begay, V, Lee, YJ, Tappe-Theodor, A, Lewin, GR, Heppenstall, PA, Taberner, FJ & Lechner, SG 2023, 'Role of TMEM100 in mechanically insensitive nociceptor un-silencing', NAT COMMUN, vol. 14, no. 1, pp. 1899. https://doi.org/10.1038/s41467-023-37602-w

APA

Nees, T. A., Wang, N., Adamek, P., Zeitzschel, N., Verkest, C., La Porta, C., Schaefer, I., Virnich, J., Balkaya, S., Prato, V., Morelli, C., Begay, V., Lee, Y. J., Tappe-Theodor, A., Lewin, G. R., Heppenstall, P. A., Taberner, F. J., & Lechner, S. G. (2023). Role of TMEM100 in mechanically insensitive nociceptor un-silencing. NAT COMMUN, 14(1), 1899. https://doi.org/10.1038/s41467-023-37602-w

Vancouver

Nees TA, Wang N, Adamek P, Zeitzschel N, Verkest C, La Porta C et al. Role of TMEM100 in mechanically insensitive nociceptor un-silencing. NAT COMMUN. 2023 Apr 5;14(1):1899. https://doi.org/10.1038/s41467-023-37602-w

Bibtex

@article{dc14e103161847419d402c890e271d6e,
title = "Role of TMEM100 in mechanically insensitive nociceptor un-silencing",
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.",
keywords = "Animals, Mice, Inflammation/metabolism, Knee Joint, Nociceptors/metabolism, Pain/metabolism, Skin/metabolism",
author = "Nees, {Timo A} and Na Wang and Pavel Adamek and Nadja Zeitzschel and Clement Verkest and {La Porta}, Carmen and Irina Schaefer and Julie Virnich and Selin Balkaya and Vincenzo Prato and Chiara Morelli and Valerie Begay and Lee, {Young Jae} and Anke Tappe-Theodor and Lewin, {Gary R} and Heppenstall, {Paul A} and Taberner, {Francisco J} and Lechner, {Stefan G}",
note = "{\textcopyright} 2023. The Author(s).",
year = "2023",
month = apr,
day = "5",
doi = "10.1038/s41467-023-37602-w",
language = "English",
volume = "14",
pages = "1899",
journal = "NAT COMMUN",
issn = "2041-1723",
publisher = "NATURE PUBLISHING GROUP",
number = "1",

}

RIS

TY - JOUR

T1 - Role of TMEM100 in mechanically insensitive nociceptor un-silencing

AU - Nees, Timo A

AU - Wang, Na

AU - Adamek, Pavel

AU - Zeitzschel, Nadja

AU - Verkest, Clement

AU - La Porta, Carmen

AU - Schaefer, Irina

AU - Virnich, Julie

AU - Balkaya, Selin

AU - Prato, Vincenzo

AU - Morelli, Chiara

AU - Begay, Valerie

AU - Lee, Young Jae

AU - Tappe-Theodor, Anke

AU - Lewin, Gary R

AU - Heppenstall, Paul A

AU - Taberner, Francisco J

AU - Lechner, Stefan G

N1 - © 2023. The Author(s).

PY - 2023/4/5

Y1 - 2023/4/5

N2 - 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.

AB - 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.

KW - Animals

KW - Mice

KW - Inflammation/metabolism

KW - Knee Joint

KW - Nociceptors/metabolism

KW - Pain/metabolism

KW - Skin/metabolism

U2 - 10.1038/s41467-023-37602-w

DO - 10.1038/s41467-023-37602-w

M3 - SCORING: Journal article

C2 - 37019973

VL - 14

SP - 1899

JO - NAT COMMUN

JF - NAT COMMUN

SN - 2041-1723

IS - 1

ER -