Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

The recovery of neurological function following spinal cord injury (SCI) is primarily constrained by two core pathological mechanisms: neuroinflammation and impaired tissue regeneration. While extracellular vesicles (EVs) have emerged as a promising therapeutic approach, their clinical translation remains limited by the inherent low bioactivity of natural EVs and suboptimal targeting efficiency at lesion sites. In this study, we developed a targeted EV delivery system with synergistic therapeutic potential, termed C-A/R-EVs, through a multidimensional engineering strategy. Specifically, the system leverages the blood-spinal cord barrier-penetrating ability of Angiopep-2 and the pathologically neovascular targeting capability of RGD to achieve precise localization in the SCI region. Additionally, a curcumin pretreatment strategy is employed to enhance the anti-inflammatory and neuroregenerative properties of the EVs. SnRNA-seq reveals that C-A/R-EVs reprogram microglia from a pro-inflammatory phenotype to a reparative phenotype, effectively suppressing neuroinflammation and promoting neural repair. Mechanistically, C-A/R-EVs facilitate axonal regeneration through enhancing the phagocytosis of myelin debris via reparative microglia, while simultaneously reducing the presence of inflammatory microglia to mitigate postinjury neuroinflammation. Moreover, C-A/R-EVs contribute to the restoration of the blood-spinal cord barrier. This study provides new insights into the design and fabrication of engineered EVs to synergistically enhance spinal cord repair through multimodal mechanisms.

Download full-text PDF

Source
http://dx.doi.org/10.1021/acsnano.5c08573DOI Listing

Publication Analysis

Top Keywords

spinal cord
12
multidimensional engineering
8
extracellular vesicles
8
targeted delivery
8
cord injury
8
blood-spinal cord
8
cord
5
engineering extracellular
4
vesicles targeted
4
delivery microglial
4

Similar Publications

Background And Objectives: Myelitis is a relatively common clinical entity for neurologists, with diverse underlying causes. The aim of this study was to describe the incidence of myelitis, its causes, clinical presentation, and factors predicting functional outcomes and relapses.

Methods: Using the Swedish National Patient Registry, we identified all adult patients in Stockholm County between 2008 and 2018 using International Classification of Diseases, 10th Edition (ICD-10) codes likely to include myelitis.

View Article and Find Full Text PDF

Study Design: A retrospective study with a crossover design.

Objectives: Maintaining mean arterial pressure (MAP) is crucial in the early management of SCI, yet the role of oral midodrine in this setting remains unclear. This study evaluates whether midodrine facilitates IV vasopressor weaning within 24 hours of initiation.

View Article and Find Full Text PDF

A considerable number of individuals are diagnosed with idiopathic trigeminal neuralgia. In order to achieve a more complete understanding of the pathophysiology, it is essential to adopt a range of novel approaches and utilize new animal models. This study investigated changes in the messenger RNA (mRNA) expression of ion-channels in a newly developed animal model of trigeminal neuropathic pain induced by cervical spinal dorsal horn compression.

View Article and Find Full Text PDF

Dual Role of DLK1 in GnRH Neuron Ontogeny.

Stem Cell Rev Rep

September 2025

Stem Cells and Metabolism Research Program (STEMM), Research Programs Unit, Faculty of Medicine, University of Helsinki, Helsinki, 00014, Finland.

Mutations in Delta Like Non-Canonical Notch Ligand 1 (DLK1), a paternally expressed imprinted gene, underlie central precocious puberty (CPP), yet the mechanism remains unclear. To test the hypothesis that DLK1 plays a role in gonadotropin releasing hormone (GnRH) neuron ontogeny, 75 base pairs were deleted in both alleles of DLK1 exon 3 with CRISPR-Cas9 in human pluripotent stem cells (hPSCs). This line, exhibiting More than 80% loss of DLK1 protein, was differentiated into GnRH neurons by dual SMAD inhibition (dSMADi), FGF8 treatment and Notch inhibition, as previously described, however, it did not exhibit accelerated GNRH1 expression.

View Article and Find Full Text PDF