ArticleMolecular neurobiology2017
Increases of Galectin-1 and its S-nitrosylated form in the Brain Tissues of Scrapie-Infected Rodent Models and Human Prion Diseases.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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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.
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Who cites it
4 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
- Association between Galectin Levels and Neurodegenerative Diseases: Systematic Review and Meta-Analysis.Biomolecules · 2022Pooled it
- Activation of Innate Immunity and Autophagy in Brain Tissues with Prion Disease and Degradation of Abnormal PrPs in Cells - China's Studies.China CDC weekly · 2022Review
- Galectins and Their Ligand Glycoconjugates in the Central Nervous System Under Physiological and Pathological Conditions.Frontiers in neuroanatomy · 2021Review
- Significant enhanced expressions of aquaporin-1, -4 and -9 in the brains of various prion diseases.Prion · 2019Article
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Galectin-1 (Gal-1) shows neuroprotective activity in brain ischemia, spinal cord injury, and autoimmune neuroinflammation. To evaluate the Gal-1 situation in the brains of prion disease, the brain levels of Gal-1 in several scrapie-infected experimental rodent models were tested by Western blot, including agents 263K-infected hamsters, 139A-, ME7-, and S15-infected mice. Remarkable increases of brain Gal-1 were observed in all tested scrapie-infected rodents at the terminal stage. The brain levels of Gal-1 showed time-dependent increases along with the prolonging of incubation times. Immunohistochemical assays illustrated much stronger stainings in the brain sections of scrapie-infected rodents. Quantitative RT-PCR of Gal-1 gene demonstrated increased transcription in the brains of scrapie-infected mice. Gal-1 was colocalized with GFAP- and NeuN-positive cells, but not with Iba-1-positive cells in immunofluorescent test. Increases of Gal-1 were also detected in the several postmortem cortex regions of human prion diseases. Moreover, the S-nitrosylated forms of Gal-1 in the brains of scrapie-infected rodents were significantly higher than those of normal ones. Our finding here demonstrates markedly increased brain Gal-1 and S-nitrosylated Gal-1 both in scrapie-infected rodents and human prion diseases.
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