Identification of Myelin Basic Protein Proximity Interactome Using TurboID Labeling Proteomics

Smirnova, Evgeniya V.; Rakitina, Tatiana V.; Ziganshin, Rustam H.; Saratov, George A.; Арапиди, Г. П.; Belogurov, A. A.; Kudriaeva, Anna

doi:10.3390/cells12060944

Cited by 3 publications

(1 citation statement)

References 129 publications

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“…5 a). Notably, the levels of MBP, key structural elements of the myelin sheath [ 33 ], were significantly decreased in mice with TBI-induced depression. Several studies have demonstrated that myelin abnormalities are closely related to the occurrence and progression of depression in both patients and mice [ 34 – 36 ].…”

Section: Resultsmentioning

confidence: 99%

FOXO1 reshapes neutrophils to aggravate acute brain damage and promote late depression after traumatic brain injury

Zhou,

Liu,

et al. 2024

Military Med Res

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Background Neutrophils are traditionally viewed as first responders but have a short onset of action in response to traumatic brain injury (TBI). However, the heterogeneity, multifunctionality, and time-dependent modulation of brain damage and outcome mediated by neutrophils after TBI remain poorly understood. Methods Using the combined single-cell transcriptomics, metabolomics, and proteomics analysis from TBI patients and the TBI mouse model, we investigate a novel neutrophil phenotype and its associated effects on TBI outcome by neurological deficit scoring and behavioral tests. We also characterized the underlying mechanisms both in vitro and in vivo through molecular simulations, signaling detections, gene expression regulation assessments [including dual-luciferase reporter and chromatin immunoprecipitation (ChIP) assays], primary cultures or co-cultures of neutrophils and oligodendrocytes, intracellular iron, and lipid hydroperoxide concentration measurements, as well as forkhead box protein O1 (FOXO1) conditional knockout mice. Results We identified that high expression of the FOXO1 protein was induced in neutrophils after TBI both in TBI patients and the TBI mouse model. Infiltration of these FOXO1high neutrophils in the brain was detected not only in the acute phase but also in the chronic phase post-TBI, aggravating acute brain inflammatory damage and promoting late TBI-induced depression. In the acute stage, FOXO1 upregulated cytoplasmic Versican (VCAN) to interact with the apoptosis regulator B-cell lymphoma-2 (BCL-2)-associated X protein (BAX), suppressing the mitochondrial translocation of BAX, which mediated the antiapoptotic effect companied with enhancing interleukin-6 (IL-6) production of FOXO1high neutrophils. In the chronic stage, the “FOXO1-transferrin receptor (TFRC)” mechanism contributes to FOXO1high neutrophil ferroptosis, disturbing the iron homeostasis of oligodendrocytes and inducing a reduction in myelin basic protein, which contributes to the progression of late depression after TBI. Conclusions FOXO1high neutrophils represent a novel neutrophil phenotype that emerges in response to acute and chronic TBI, which provides insight into the heterogeneity, reprogramming activity, and versatility of neutrophils in TBI.

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Section: Resultsmentioning

confidence: 99%

FOXO1 reshapes neutrophils to aggravate acute brain damage and promote late depression after traumatic brain injury

Zhou,

Liu,

et al. 2024

Military Med Res

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Myelin basic protein antagonizes the SARS-CoV-2 protein ORF3a-induced autophagy inhibition

Saratov,

Belogurov,

Kudriaeva

2024

Biochimie

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Diverse functions of DEAD‐box proteins in oligodendrocyte development, differentiation, and homeostasis

Bizen,

Takebayashi

2024

Journal of Neurochemistry

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Oligodendrocytes, a type of glial cell in the central nervous system, have a critical role in the formation of myelin around axons, facilitating saltatory conduction, and maintaining the integrity of nerve axons. The dysregulation of oligodendrocyte differentiation and homeostasis have been implicated in a wide range of neurological diseases, including dysmyelinating disorders (e.g., Pelizaeus‐Merzbacher disease), demyelinating diseases (e.g., multiple sclerosis), Alzheimer's disease, and psychiatric disorders. Therefore, unraveling the mechanisms of oligodendrocyte development, differentiation, and homeostasis is essential for understanding the pathogenesis of these diseases and the development of therapeutic interventions. Numerous studies have identified and analyzed the functions of transcription factors, RNA metabolic factors, translation control factors, and intracellular and extracellular signals involved in the series of processes from oligodendrocyte fate determination to terminal differentiation. DEAD‐box proteins, multifunctional RNA helicases that regulate various intracellular processes, including transcription, RNA processing, and translation, are increasingly recognized for their diverse roles in various aspects of oligodendrocyte development, differentiation, and maintenance of homeostasis. This review introduces the latest insights into the regulatory networks of oligodendrocyte biology mediated by DEAD‐box proteins.image

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Identification of Myelin Basic Protein Proximity Interactome Using TurboID Labeling Proteomics

Cited by 3 publications

References 129 publications

FOXO1 reshapes neutrophils to aggravate acute brain damage and promote late depression after traumatic brain injury

FOXO1 reshapes neutrophils to aggravate acute brain damage and promote late depression after traumatic brain injury

Myelin basic protein antagonizes the SARS-CoV-2 protein ORF3a-induced autophagy inhibition

Diverse functions of DEAD‐box proteins in oligodendrocyte development, differentiation, and homeostasis

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