Neuron myelination is accelerated by Bruton's tyrosine kinase inhibition via microglial extracellular vesicles.
5 affiliations
- 1Department of Physiology and Pharmacology, Sapienza University of Rome, Rome, Italy.
- 2Department of Human Neurosciences, Sapienza University of Rome, Rome, Italy.
- 3Institute of Biomedical Technologies, CNR, Segrate, Italy.
- 4IRCCS Neuromed, Pozzilli, Italy.
- 5Department of Physiology and Pharmacology, Laboratory Affiliated to Istituto Pasteur Italia Fondazione Cenci Bolognetti, Sapienza University, Rome, Italy.
Abstract
The altered myelin repair observed in demyelinating diseases such as multiple sclerosis (MS) potentially exposes axons to various stressors, with consequent neurodegeneration. Preclinical evidence has demonstrated that Bruton's tyrosine kinase inhibitors (BTKi), such as ibrutinib, delay MS progression by acting on myeloid cells. We investigated the effects of ibrutinib on remyelination using a novel in vitro model of spinal cord neurons derived from postnatal mice. We demonstrated that (1) spinal cord neuron cells represent a suitable model for investigating myelination following L‑α‑lysophosphatidylcholine (LPC) treatment; (2) ibrutinib induces remyelination and reduces stathmin‑1 expression in spinal cord cultures; and (3) ibrutinib reduces the inflammatory phenotype of microglia‑like BV2 cells, thereby modulating the expression of miR‑223 in extracellular vesicles (EVs). Altogether, these data pave the way for a better understanding of the mechanisms underlying remyelination following ibrutinib treatment and support the hypothesis that EV‑derived microglial cells play a key role.
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BibTeX
@article{tartaglia2026neuron,
title = {{Neuron myelination is accelerated by Bruton's tyrosine kinase inhibition via microglial extracellular vesicles.}},
author = {Matteo Tartaglia and Arianna Ioni and Mariassunta De Luca and Laura Vilardo and Igea D'Agnano and Antonella Conte and Cristina Limatola and Myriam Catalano},
journal = {Frontiers in cellular neuroscience},
year = {2026},
month = oct,
doi = {10.3389/fncel.2026.1864654},
url = {https://europepmc.org/article/MED/42952672},
note = {CC BY},
}
RIS
TY - JOUR
TI - Neuron myelination is accelerated by Bruton's tyrosine kinase inhibition via microglial extracellular vesicles.
AU - Matteo Tartaglia
AU - Arianna Ioni
AU - Mariassunta De Luca
AU - Laura Vilardo
AU - Igea D'Agnano
AU - Antonella Conte
AU - Cristina Limatola
AU - Myriam Catalano
PY - 2026
DA - 2026/10/14
JO - Frontiers in cellular neuroscience
DO - 10.3389/fncel.2026.1864654
UR - https://europepmc.org/article/MED/42952672
AB - The altered myelin repair observed in demyelinating diseases such as multiple sclerosis (MS) potentially exposes axons to various stressors, with consequent neurodegeneration. Preclinical evidence has demonstrated that Bruton's tyrosine kinase inhibitors (BTKi), such as ibrutinib, delay MS progression by acting on myeloid cells. We investigated the effects of ibrutinib on remyelination using a novel in vitro model of spinal cord neurons derived from postnatal mice. We demonstrated that (1) spinal cord neuron cells represent a suitable model for investigating myelination following L‑α‑lysophosphatidylcholine (LPC) treatment; (2) ibrutinib induces remyelination and reduces stathmin‑1 expression in spinal cord cultures; and (3) ibrutinib reduces the inflammatory phenotype of microglia‑like BV2 cells, thereby modulating the expression of miR‑223 in extracellular vesicles (EVs). Altogether, these data pave the way for a better understanding of the mechanisms underlying remyelination following ibrutinib treatment and support the hypothesis that EV‑derived microglial cells play a key role.
SN - 1662-5102
ER -