Myelin Biology

Bolino, Alessandra

doi:10.1007/s13311-021-01083-w

Cited by 13 publications

(4 citation statements)

References 134 publications

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“…During this process, Schwann cells must alter their gene expression, assuming a repair phenotype that is distinct from pro-myelinating immature Schwann cells [19,27]. Throughout development, myelination and repair, Schwann cells constitutively express sox10 (SRY-box transcription factor 10), a powerful transcription factor determining Schwann cell identity [28]. During the initiation of myelination in development, sox10 activates other key transcription factors, like Oct6, to turn on the expression of myelin proteins, such as myelin protein zero (MPZ) and myelin basic protein (MPB) [20].…”

Section: Discussionmentioning

confidence: 99%

Radiopaque Implantable Biomaterials for Nerve Repair

Pawelec

Hix

Shapiro

2023

Preprint

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Repairing peripheral nerve injuries remains a clinical challenge. To enhance nerve regeneration and functional recovery, the use of auxiliary implantable biomaterial conduits has become widespread. After implantation, there is currently no way to assess the location or function of polymeric biomedical devices, as they cannot be easily differentiated from surrounding tissue using clinical imaging modalities. Adding nanoparticle contrast agents into polymer matrices can introduce radiopacity and enable imaging using computed tomography (CT), but radiopacity must be balanced with changes in material properties that impact device function and biological response. In this study radiopacity was introduced to porous films of polycaprolactone (PCL) and poly(lactide-co-glycolide) (PLGA) 50:50 and 85:15 with 0-40wt% biocompatible tantalum oxide (TaOx) nanoparticles. To achieve radiopacity, at least 5wt% TaOx was required, with more than or equal to 20wt% TaOx leading to reduced mechanical properties and increased nano-scale surface roughness of films. As polymers used for peripheral nerve injury devices, films facilitated nerve regeneration in an in vitro co-culture model of glia (Schwann cells) and dorsal root ganglion neurons (DRG), measured by expression markers for myelination. The ability of radiopaque films to support nerve regeneration was determined by the properties of the polymer matrix, with a range of 5-20wt% TaOx balancing both imaging functionality with biological response and proving that in situ monitoring of nerve repair devices is feasible.

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Section: Discussionmentioning

confidence: 99%

Radiopaque Implantable Biomaterials for Nerve Repair

Pawelec

Hix

Shapiro

2023

Preprint

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“…Myelin is a crucial evolutionary acquisition and adaptation, which supports the development of complex nervous systems in all vertebrates 99 , 100 . Myelin plasticity has emerged as a potential modulator of neuronal circuits, and the process of new myelin sheath formation, or myelination, is facilitated by certain neuroglia such as oligodendrocytes and schwann cells 101 , 102 .…”

Section: Discussionmentioning

confidence: 99%

“…In the central nervous system, oligodendrocytes differentiated from OPCs produce the myelin sheath wrapped around the neuronal axons, whereas Schwann cells myelinating axons in the peripheral nervous system 102 . Myelination not only enables the rapid and efficient transmission of electric impulses along the axon but also regulates axonal metabolism and neural plasticity 100 , 103 . Under normal conditions, myelination occurs throughout the life course and plays a critical role in the regulation of cognitive and other behavioral functions 104 .…”

Section: Discussionmentioning

confidence: 99%

Photobiomodulation attenuates oligodendrocyte dysfunction and prevents adverse neurological consequences in a rat model of early life adversity

Huang¹,

Zhang²,

Ma³

et al. 2023

Theranostics

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Rationale: Adverse experiences in early life including abuse, trauma and neglect, have been linked to poor physical and mental health outcomes. Emerging evidence implies that those who experienced early life adversity (ELA) are more likely to develop cognitive dysfunction and depressive-like symptoms in adulthood. The molecular mechanisms responsible for the negative consequences of ELA, however, remain unclear. In the absence of effective management options, anticipatory guidance is the mainstay of ELA prevention. Furthermore, there is no available treatment that prevents or alleviates the neurologic sequelae of ELA, especially traumatic stress. Hence, the present study aims to investigate the mechanisms for these associations and evaluate whether photobiomodulation (PBM), a non-invasive therapeutic procedure, can prevent the negative cognitive and behavioral manifestations of ELA in later life. Methods: ELA was induced by repeated inescapable electric foot shock of rats from postnatal day 21 to 26. On the day immediately following the last foot shock, 2-min daily PBM treatment was applied transcranially for 7 consecutive days. Cognitive dysfunction and depression-like behaviors were measured by a battery of behavioral tests in adulthood. Subsequently, oligodendrocyte progenitor cells (OPCs) differentiation, the proliferation and apoptosis of oligodendrocyte lineage cells (OLs), mature oligodendrocyte, myelinating oligodendrocyte, the level of oxidative damage, reactive oxygen species (ROS) and total antioxidant capacity were measured and analyzed using immunofluorescence staining, capillary-based immunoassay (ProteinSimple®) and antioxidant assay kit. Results: The rats exposed to ELA exhibited obvious oligodendrocyte dysfunction, including a reduction in OPCs differentiation, diminished generation and survival of OLs, decreased OLs, and decreased matured oligodendrocyte. Furthermore, a deficit in myelinating oligodendrocytes was observed, in conjunction with an imbalance in redox homeostasis and accumulated oxidative damage. These alternations were concomitant with cognitive dysfunction and depression-like behaviors. Importantly, we found that early PBM treatment largely prevented these pathologies and reversed the neurologic sequelae resulting from ELA. Conclusions: Collectively, these findings provide new insights into the mechanism by which ELA affects neurological outcomes. Moreover, our findings support that PBM may be a promising strategy to prevent ELA-induced neurologic sequelae that develops later in life.

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“…In the event that an axon is destroyed, myelin can help direct the regeneration of the damaged axon. In the demyelinating disease, the nutritional support provided by myelin is essential for the survival of axons ( Suminaite et al, 2019 ; Bolino, 2021 ).…”

Section: Cellular Repair Mechanisms Of Spinal Cord Injurymentioning

confidence: 99%

Restoration of spinal cord injury: From endogenous repairing process to cellular therapy

Tang

Zhang

et al. 2022

Front. Cell. Neurosci.

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Spinal cord injury (SCI) disrupts neurological pathways and impacts sensory, motor, and autonomic nerve function. There is no effective treatment for SCI currently. Numerous endogenous cells, including astrocytes, macrophages/microglia, and oligodendrocyte, are involved in the histological healing process following SCI. By interfering with cells during the SCI repair process, some advancements in the therapy of SCI have been realized. Nevertheless, the endogenous cell types engaged in SCI repair and the current difficulties these cells confront in the therapy of SCI are poorly defined, and the mechanisms underlying them are little understood. In order to better understand SCI and create new therapeutic strategies and enhance the clinical translation of SCI repair, we have comprehensively listed the endogenous cells involved in SCI repair and summarized the six most common mechanisms involved in SCI repair, including limiting the inflammatory response, protecting the spared spinal cord, enhancing myelination, facilitating neovascularization, producing neurotrophic factors, and differentiating into neural/colloidal cell lines.

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Myelin Biology

Cited by 13 publications

References 134 publications

Radiopaque Implantable Biomaterials for Nerve Repair

Radiopaque Implantable Biomaterials for Nerve Repair

Photobiomodulation attenuates oligodendrocyte dysfunction and prevents adverse neurological consequences in a rat model of early life adversity

Restoration of spinal cord injury: From endogenous repairing process to cellular therapy

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