ArticleJournal of neuroscience research2015
Reductions in kinesin expression are associated with nitric oxide-induced axonal damage.
Article in Journal of neuroscience research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed, 25 citations in OpenAlex.
- How does Nogo receptor influence demyelination and remyelination in the context of multiple sclerosis?Frontiers in cellular neuroscience · 2023Review
- Multimodal Assessment of Bottlenose Dolphin Auditory Nuclei Using 7-Tesla MRI, Immunohistochemistry and Stereology.Veterinary sciences · 2022Article
- Nitrosative stress in Parkinson's disease.NPJ Parkinson's disease · 2022Review
- Reduced expression of mitochondrial fumarate hydratase in progressive multiple sclerosis contributes to impaired in vitro mesenchymal stromal cell-mediated neuroprotection.Multiple sclerosis (Houndmills, Basingstoke, England) · 2022Article
- Cytoskeletal Arrest: An Anoxia Tolerance Mechanism.Metabolites · 2021Review
- KIF5A and the contribution of susceptibility genotypes as a predictive biomarker for multiple sclerosis.Journal of neurology · 2021Article
- Calpain mediated expansion of CD4+ cytotoxic T cells in rodent models of Parkinson's disease.Experimental neurology · 2020Article
- Nystatin Regulates Axonal Extension and Regeneration by Modifying the Levels of Nitric Oxide.Frontiers in molecular neuroscience · 2020Article
- shRNA-mediated PPARα knockdown in human glioma stem cells reduces in vitro proliferation and inhibits orthotopic xenograft tumour growth.The Journal of pathology · 2019Article
- Dysregulation of Mesenchymal Stromal Cell Antioxidant Responses in Progressive Multiple Sclerosis.Stem cells translational medicine · 2018Article
- Reduced neuroprotective potential of the mesenchymal stromal cell secretome with ex vivo expansion, age and progressive multiple sclerosis.Cytotherapy · 2018Article
- Association between low thyroid-stimulating hormone, posterior cortical atrophy and nitro-oxidative stress in elderly patients with cognitive dysfunction.Archives of medical science : AMS · 2017Article
- Regulation of cytoskeletal dynamics by redox signaling and oxidative stress: implications for neuronal development and trafficking.Frontiers in cellular neuroscience · 2015Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Axonal injury is often characterized by axonal transport defects and abnormal accumulation of intra-axonal components. Nitric oxide (NO) has a key role in mediating inflammatory axonopathy in many neurodegenerative diseases, but little is known about how nitrosative/oxidative stress affects axonal transport or whether reductions in kinesin superfamily protein (KIF) expression correlate with axon pathology. KIFs are molecular motors that have a key role in axonal and dendritic transport, and impairment of these mechanisms has been associated with a number of neurological disorders. This study shows that rat cortical neurons exposed to NO display both a time-dependent decrease in KIF gene/protein expression and neurofilament phosphorylation in addition to a reduction in axonal length and neuronal survival. Because mesenchymal stem cells (MSCs) represent a promising therapeutic candidate for neuronal/axonal repair, this study analyzes the capacity of MSCs to protect neurons and axonal transport mechanisms from NO damage. Results show that coculture of MSCs with NO-exposed neurons results in the preservation of KIF expression, axonal length, and neuronal survival. Altogether, these results suggest a potential mechanism involved in the disruption of axonal transport and abnormal accumulation of proteins in axons during nitrosative insult. We hypothesize that impaired axonal transport contributes, per se, to progression of injury and provide further evidence of the therapeutic potential of MSCs for neurodegenerative disorders.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.