Myelination- and migration-associated genes are downregulated after phagocytosis in cultured oligodendrocyte precursor cells.


Journal

Journal of neurochemistry
ISSN: 1471-4159
Titre abrégé: J Neurochem
Pays: England
ID NLM: 2985190R

Informations de publication

Date de publication:
Nov 2023
Historique:
revised: 19 09 2023
received: 07 12 2022
accepted: 25 09 2023
medline: 13 11 2023
pubmed: 24 10 2023
entrez: 24 10 2023
Statut: ppublish

Résumé

In the central nervous system, microglia are responsible for removing infectious agents, damaged/dead cells, and amyloid plaques by phagocytosis. Other cell types, such as astrocytes, are also recently recognized to show phagocytotic activity under some conditions. Oligodendrocyte precursor cells (OPCs), which belong to the same glial cell family as microglia and astrocytes, may have similar functions. However, it remains largely unknown whether OPCs exhibit phagocytic activity against foreign materials like microglia. To answer this question, we examined the phagocytosis activity of OPCs using primary rat OPC cultures. Since innate phagocytosis activity could trigger cell death pathways, we also investigated whether participating in phagocytosis activity may lead to OPC cell death. Our data shows that cultured OPCs phagocytosed myelin-debris-rich lysates prepared from rat corpus callosum, without progressing to cell death. In contrast to OPCs, mature oligodendrocytes did not show phagocytotic activity against the bait. OPCs also exhibited phagocytosis towards lysates of rat brain cortex and cell membrane debris from cultured astrocytes, but the percentage of OPCs that phagocytosed beta-amyloid was much lower than the myelin debris. We then conducted RNA-seq experiments to examine the transcriptome profile of OPC cultures and found that myelination- and migration-associated genes were downregulated 24 h after phagocytosis. On the other hand, there were a few upregulated genes in OPCs 24 h after phagocytosis. These data confirm that OPCs play a role in debris removal and suggest that OPCs may remain in a quiescent state after phagocytosis.

Identifiants

pubmed: 37874764
doi: 10.1111/jnc.15994
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

571-581

Subventions

Organisme : NIH HHS
Pays : United States
Organisme : NIH HHS
Pays : United States

Informations de copyright

© 2023 International Society for Neurochemistry.

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Auteurs

Gen Hamanaka (G)

Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Massachusetts, Boston, USA.

Iván Coto Hernández (IC)

Surgical Photonics and Engineering Laboratory, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA.

Hajime Takase (H)

Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Massachusetts, Boston, USA.

Hidehiro Ishikawa (H)

Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Massachusetts, Boston, USA.

Fouzi Benboujja (F)

Department of Otolaryngology Head and Neck Surgery, Massachusetts Eye and Ear, Harvard Medical School, Boston, Massachusetts, USA.

Shintaro Kimura (S)

Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Massachusetts, Boston, USA.

Norito Fukuda (N)

Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Massachusetts, Boston, USA.

Shuzhen Guo (S)

Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Massachusetts, Boston, USA.

Josephine Lok (J)

Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Massachusetts, Boston, USA.

Eng H Lo (EH)

Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Massachusetts, Boston, USA.

Ken Arai (K)

Neuroprotection Research Laboratories, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Massachusetts, Boston, USA.

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