Role of integrin αvβ5 receptor and microglia in delayed-onset muscle soreness in mice.
4 affiliations
- 1Laboratory of Neuroimmunobiology of Pain, Center for Experimental Biology, Federal University of Alfenas, Alfenas, 37131-001, Minas Gerais, Brazil.
- 2Inflammation and Exercise Immunology Laboratory (LABIIEX), Federal University of Ouro Preto Sports Center, Ouro Preto, 35400-000, MG, Brazil.
- 3Laboratory of Pain and Analgesia, Pharmacology Department, Federal University of Minas Gerais, Belo Horizonte, 31270-901, Minas Gerais, Brazil.
- 4Laboratory of Neuroimmunobiology of Pain, Center for Experimental Biology, Federal University of Alfenas, Alfenas, 37131-001, Minas Gerais, Brazil. [email protected].
Abstract
Delayed-onset muscle soreness (DOMS) is characterized by muscle pain, stiffness, and tenderness following intense or unaccustomed exercise. In humans, symptoms typically arise 6-72 h post-exercise. This study investigated a novel mechanism underlying DOMS, focusing on the involvement of the irisin receptor integrin αvβ5 and spinal microglia in its development. Male C57BL/6 mice were subjected to a DOMS model induced by an acute aerobic exercise protocol, and nociceptive thresholds were assessed using the von Frey filament test. The role of spinal integrin αvβ5 was evaluated via intrathecal administration of the antagonist cilengitide, given both prior to exercise and 24 h post-exercise. To assess irisin's nociceptive effects, it was also administered intrathecally. Additionally, minocycline, a microglial inhibitor, was administered before irisin to determine microglial involvement. An in vitro assay evaluated microglial activation by irisin via flow cytometry. Pro- and anti-inflammatory cytokines were quantified by ELISA. Cilengitide reversed exercise-induced DOMS and reduced spinal pro-inflammatory cytokines. Irisin induced nociception, which was attenuated by minocycline. Irisin also activated microglia in vitro, increasing pro-inflammatory cytokine production. These findings suggest integrin αvβ5 and spinal microglia play critical roles in DOMS pathogenesis, with irisin and pro-inflammatory cytokines as key mediators.
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BibTeX
@article{rocha2026role,
title = {{Role of integrin αvβ5 receptor and microglia in delayed-onset muscle soreness in mice.}},
author = {Bruno Lopes Gonçalves Rocha and Flavio Protasio Veras and Rafaela Silva Dos Santos and Albená Nunes-Silva and Thiago Roberto Lima Romero and Giovane Galdino},
journal = {Journal of muscle research and cell motility},
year = {2026},
month = oct,
doi = {10.1007/s10974-026-09742-1},
url = {https://europepmc.org/article/MED/42909689},
note = {CC BY},
}
RIS
TY - JOUR
TI - Role of integrin αvβ5 receptor and microglia in delayed-onset muscle soreness in mice.
AU - Bruno Lopes Gonçalves Rocha
AU - Flavio Protasio Veras
AU - Rafaela Silva Dos Santos
AU - Albená Nunes-Silva
AU - Thiago Roberto Lima Romero
AU - Giovane Galdino
PY - 2026
DA - 2026/10/23
JO - Journal of muscle research and cell motility
DO - 10.1007/s10974-026-09742-1
UR - https://europepmc.org/article/MED/42909689
AB - Delayed-onset muscle soreness (DOMS) is characterized by muscle pain, stiffness, and tenderness following intense or unaccustomed exercise. In humans, symptoms typically arise 6-72 h post-exercise. This study investigated a novel mechanism underlying DOMS, focusing on the involvement of the irisin receptor integrin αvβ5 and spinal microglia in its development. Male C57BL/6 mice were subjected to a DOMS model induced by an acute aerobic exercise protocol, and nociceptive thresholds were assessed using the von Frey filament test. The role of spinal integrin αvβ5 was evaluated via intrathecal administration of the antagonist cilengitide, given both prior to exercise and 24 h post-exercise. To assess irisin's nociceptive effects, it was also administered intrathecally. Additionally, minocycline, a microglial inhibitor, was administered before irisin to determine microglial involvement. An in vitro assay evaluated microglial activation by irisin via flow cytometry. Pro- and anti-inflammatory cytokines were quantified by ELISA. Cilengitide reversed exercise-induced DOMS and reduced spinal pro-inflammatory cytokines. Irisin induced nociception, which was attenuated by minocycline. Irisin also activated microglia in vitro, increasing pro-inflammatory cytokine production. These findings suggest integrin αvβ5 and spinal microglia play critical roles in DOMS pathogenesis, with irisin and pro-inflammatory cytokines as key mediators.
SN - 0142-4319
SN - 1573-2657
ER -