Glial and neuroimmune cell choreography in sexually dimorphic pain signaling

Midavaine, Élora; Côté, Jérôme; Marchand, Serge; Sarret, Philippe

doi:10.1016/j.neubiorev.2021.01.023

Cited by 38 publications

(22 citation statements)

References 333 publications

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“…Recent findings have highlighted a sexual dimorphism in glial and immune cell responses present in pain signalling (for review, see Midavaine et al, 2021); thus, future investigations of the sex-dependent glial response and its crosstalk with immune cells, following SCI, are of great interest. The analysis of cellular dynamics following SCI in different contexts (species, age, sex, etc.)…”

Section: Concluding Comments and Future Directionsmentioning

confidence: 99%

Dynamic Diversity of Glial Response Among Species in Spinal Cord Injury

Perez

Gerber

Perrin

2021

Front. Aging Neurosci.

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The glial scar that forms after traumatic spinal cord injury (SCI) is mostly composed of microglia, NG2 glia, and astrocytes and plays dual roles in pathophysiological processes induced by the injury. On one hand, the glial scar acts as a chemical and physical obstacle to spontaneous axonal regeneration, thus preventing functional recovery, and, on the other hand, it partly limits lesion extension. The complex activation pattern of glial cells is associated with cellular and molecular crosstalk and interactions with immune cells. Interestingly, response to SCI is diverse among species: from amphibians and fishes that display rather limited (if any) glial scarring to mammals that exhibit a well-identifiable scar. Additionally, kinetics of glial activation varies among species. In rodents, microglia become activated before astrocytes, and both glial cell populations undergo activation processes reflected amongst others by proliferation and migration toward the injury site. In primates, glial cell activation is delayed as compared to rodents. Here, we compare the spatial and temporal diversity of the glial response, following SCI amongst species. A better understanding of mechanisms underlying glial activation and scar formation is a prerequisite to develop timely glial cell-specific therapeutic strategies that aim to increase functional recovery.

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Section: Concluding Comments and Future Directionsmentioning

confidence: 99%

Dynamic Diversity of Glial Response Among Species in Spinal Cord Injury

Perez

Gerber

Perrin

2021

Front. Aging Neurosci.

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“…46 Interestingly, and perhaps relevant for headache observed after MTBI, is that signaling mechanisms underlying pain hypersensitivity (eg, glial cell activation) are sexually dimorphic. 47,48 Further adding to the complexity, not only gender but also perceptions of gender inequality are associated www.archives-pmr.org with psychological distress. 49 Future studies should further target how sex and gender influence outcome after MTBI.…”

Section: Discussionmentioning

confidence: 99%

Trajectories of Persistent Postconcussion Symptoms and Factors Associated With Symptom Reporting After Mild Traumatic Brain Injury

Fordal

Stenberg

Saksvik

et al. 2022

Archives of Physical Medicine and Rehabilitation

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“…However, only one sex of the mice (male) was used in this study. Sex‐specific susceptibility to pain conditions as well as sex differences in pain sensitivity, pain tolerance, and analgesic efficacy are increasingly recognized in the literature and have thus prompted scientists to seek mechanistic explanations (Midavaine et al., 2021 ). Therefore, it is necessary to investigated potential sex‐based differences in the process of TN in the future work.…”

Section: Discussionmentioning

confidence: 99%

MiR‐223‐3p alleviates trigeminal neuropathic pain in the male mouse by targeting MKNK2 and MAPK/ERK signaling

et al. 2022

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Background: Trigeminal neuralgia (TN) is a neuropathic pain that occurs in branches of the trigeminal nerve. MicroRNAs (miRNAs) have been considered key mediators of neuropathic pain. This study was aimed to elucidate the pathophysiological function and mechanisms of miR-223-3p in mouse models of TN. Methods: Infraorbital nerve chronic constriction injury (CCI-ION) was applied in male C57BL/6J mice to establish mouse models of TN. Pain responses were assessed utilizing Von Frey method. The expression of miR-223-3p, MKNK2, and MAPK/ERK pathway protein in trigeminal ganglions (TGs) of CCI-ION mice was measured using RT-qPCR and Western blotting. The concentrations of inflammatory cytokines were evaluated using Western blotting. The relationship between miR-223-3p and MKNK2 was tested by a luciferase reporter assay. Results: We found that miR-223-3p was downregulated, while MKNK2 was upregulated in TGs of CCI-ION mice. MiR-223-3p overexpression by an intracerebroventricular injection of Lv-miR-223-3p attenuated trigeminal neuropathic pain in CCI-ION mice, as well as reduced the protein levels of pro-inflammatory cytokines in TGs of CCI-ION mice. MKNK2 was verified to be targeted by miR-223-3p. Additionally, miR-223-3p overexpression decreased the phosphorylation levels of ERK1/2, JNK, and p38 protein in TGs of CCI-ION mice to inhibit MAPK/ERK signaling. Conclusions: Overall, miR-223-3p attenuates the development of TN by targeting MKNK2 to suppress MAPK/ERK signaling.

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Glial and neuroimmune cell choreography in sexually dimorphic pain signaling

Cited by 38 publications

References 333 publications

Dynamic Diversity of Glial Response Among Species in Spinal Cord Injury

Dynamic Diversity of Glial Response Among Species in Spinal Cord Injury

Trajectories of Persistent Postconcussion Symptoms and Factors Associated With Symptom Reporting After Mild Traumatic Brain Injury

MiR‐223‐3p alleviates trigeminal neuropathic pain in the male mouse by targeting MKNK2 and MAPK/ERK signaling

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