Aarhus University Seal

Jens Randel Nyengaard

Demise of nociceptive Schwann cells causes nerve retraction and pain hyperalgesia

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Standard

Demise of nociceptive Schwann cells causes nerve retraction and pain hyperalgesia. / Rinwa, Puneet; Calvo-Enrique, Laura; Zhang, Ming-Dong et al.

In: Pain, Vol. 162, No. 6, 06.2021, p. 1816-1827.

Research output: Contribution to journal/Conference contribution in journal/Contribution to newspaperJournal articleResearchpeer-review

Harvard

APA

CBE

MLA

Vancouver

Rinwa P, Calvo-Enrique L, Zhang M-D, Nyengaard JR, Karlsson P, Ernfors P. Demise of nociceptive Schwann cells causes nerve retraction and pain hyperalgesia. Pain. 2021 Jun;162(6):1816-1827. doi: 10.1097/j.pain.0000000000002169

Author

Rinwa, Puneet ; Calvo-Enrique, Laura ; Zhang, Ming-Dong et al. / Demise of nociceptive Schwann cells causes nerve retraction and pain hyperalgesia. In: Pain. 2021 ; Vol. 162, No. 6. pp. 1816-1827.

Bibtex

@article{49df8c0f8a194331bc02d8b11e106221,
title = "Demise of nociceptive Schwann cells causes nerve retraction and pain hyperalgesia",
abstract = "ABSTRACT: Recent findings indicate that nociceptive nerves are not {"}free{"}, but similar to touch and pressure sensitive nerves, terminate in an end-organ in mice. This sensory structure consists of the nociceptive nerves and specialized nociceptive Schwann cells forming a mesh-like organ in subepidermis with pain transduction initiated at both these cellular constituents. The intimate relation of nociceptive nerves with nociceptive Schwann cells in mice raises the question whether defects in nociceptive Schwann cells can by itself contribute to pain hyperalgesia, nerve retraction, and peripheral neuropathy. We therefore examined the existence of nociceptive Schwann cells in human skin and their possible contribution to neuropathy and pain hyperalgesia in mouse models. Similar to mouse, human skin contains SOX10+/S100B+/AQP1+ Schwann cells in the subepidermal border that have extensive processes, which are intimately associated with nociceptive nerves projecting into epidermis. The ablation of nociceptive Schwann cells in mice resulted in nerve retraction and mechanical, cold, and heat hyperalgesia. Conversely, ablating the nociceptive nerves led to a retraction of epidermal Schwann cell processes, changes in nociceptive Schwann cell soma morphology, heat analgesia, and mechanical hyperalgesia. Our results provide evidence for a nociceptive sensory end-organ in the human skin and using animal models highlight the interdependence of the nerve and the nociceptive Schwann cell. Finally, we show that demise of nociceptive Schwann cells is sufficient to cause neuropathic-like pain in the mouse.",
author = "Puneet Rinwa and Laura Calvo-Enrique and Ming-Dong Zhang and Nyengaard, {Jens Randel} and P{\'a}ll Karlsson and Patrik Ernfors",
note = "Copyright {\textcopyright} 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Association for the Study of Pain.",
year = "2021",
month = jun,
doi = "10.1097/j.pain.0000000000002169",
language = "English",
volume = "162",
pages = "1816--1827",
journal = "Pain",
issn = "0304-3959",
publisher = "IASP Press",
number = "6",

}

RIS

TY - JOUR

T1 - Demise of nociceptive Schwann cells causes nerve retraction and pain hyperalgesia

AU - Rinwa, Puneet

AU - Calvo-Enrique, Laura

AU - Zhang, Ming-Dong

AU - Nyengaard, Jens Randel

AU - Karlsson, Páll

AU - Ernfors, Patrik

N1 - Copyright © 2021 The Author(s). Published by Wolters Kluwer Health, Inc. on behalf of the International Association for the Study of Pain.

PY - 2021/6

Y1 - 2021/6

N2 - ABSTRACT: Recent findings indicate that nociceptive nerves are not "free", but similar to touch and pressure sensitive nerves, terminate in an end-organ in mice. This sensory structure consists of the nociceptive nerves and specialized nociceptive Schwann cells forming a mesh-like organ in subepidermis with pain transduction initiated at both these cellular constituents. The intimate relation of nociceptive nerves with nociceptive Schwann cells in mice raises the question whether defects in nociceptive Schwann cells can by itself contribute to pain hyperalgesia, nerve retraction, and peripheral neuropathy. We therefore examined the existence of nociceptive Schwann cells in human skin and their possible contribution to neuropathy and pain hyperalgesia in mouse models. Similar to mouse, human skin contains SOX10+/S100B+/AQP1+ Schwann cells in the subepidermal border that have extensive processes, which are intimately associated with nociceptive nerves projecting into epidermis. The ablation of nociceptive Schwann cells in mice resulted in nerve retraction and mechanical, cold, and heat hyperalgesia. Conversely, ablating the nociceptive nerves led to a retraction of epidermal Schwann cell processes, changes in nociceptive Schwann cell soma morphology, heat analgesia, and mechanical hyperalgesia. Our results provide evidence for a nociceptive sensory end-organ in the human skin and using animal models highlight the interdependence of the nerve and the nociceptive Schwann cell. Finally, we show that demise of nociceptive Schwann cells is sufficient to cause neuropathic-like pain in the mouse.

AB - ABSTRACT: Recent findings indicate that nociceptive nerves are not "free", but similar to touch and pressure sensitive nerves, terminate in an end-organ in mice. This sensory structure consists of the nociceptive nerves and specialized nociceptive Schwann cells forming a mesh-like organ in subepidermis with pain transduction initiated at both these cellular constituents. The intimate relation of nociceptive nerves with nociceptive Schwann cells in mice raises the question whether defects in nociceptive Schwann cells can by itself contribute to pain hyperalgesia, nerve retraction, and peripheral neuropathy. We therefore examined the existence of nociceptive Schwann cells in human skin and their possible contribution to neuropathy and pain hyperalgesia in mouse models. Similar to mouse, human skin contains SOX10+/S100B+/AQP1+ Schwann cells in the subepidermal border that have extensive processes, which are intimately associated with nociceptive nerves projecting into epidermis. The ablation of nociceptive Schwann cells in mice resulted in nerve retraction and mechanical, cold, and heat hyperalgesia. Conversely, ablating the nociceptive nerves led to a retraction of epidermal Schwann cell processes, changes in nociceptive Schwann cell soma morphology, heat analgesia, and mechanical hyperalgesia. Our results provide evidence for a nociceptive sensory end-organ in the human skin and using animal models highlight the interdependence of the nerve and the nociceptive Schwann cell. Finally, we show that demise of nociceptive Schwann cells is sufficient to cause neuropathic-like pain in the mouse.

U2 - 10.1097/j.pain.0000000000002169

DO - 10.1097/j.pain.0000000000002169

M3 - Journal article

C2 - 33979318

VL - 162

SP - 1816

EP - 1827

JO - Pain

JF - Pain

SN - 0304-3959

IS - 6

ER -