ArticleNeural regeneration research2014
Amyloid precursor-like protein 2 C-terminal fragments upregulate S100A9 gene and protein expression in BV2 cells.
Article in Neural regeneration research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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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Who cites it
3 citing papers in PubMed, 7 citations in OpenAlex.
- Effect of Proinflammatory S100A9 Protein on Migration and Proliferation of Microglial Cells.Journal of molecular neuroscience : MN · 2023Article
- Bridging the Gap Between Fluid Biomarkers for Alzheimer's Disease, Model Systems, and Patients.Frontiers in aging neuroscience · 2020Review
- S100 Proteins in Alzheimer's Disease.Frontiers in neuroscience · 2019Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The murine microglial cell line BV2 has neuroprotective effects, but is toxic to neurons by secreting inflammatory cytokines, and is an important target in the treatment of nerve inflammation and neurodegenerative diseases. In the present study, we observed the effects of transfecting three amyloid precursor-like protein 2 (APLP2) C-terminal fragments (CTFs; C57, C50 and C31) in the pEGFP-N1 vector on S100A9 expression in BV2 cells. Reverse transcription-PCR, western blot assay and immunocytochemistry revealed that S100A9 protein and mRNA expression was greater in BV2 cells after CTF transfection than after mock transfection with an empty vector. Furthermore, transfection of full-length APLP2-751 resulted in low levels of S100A9 protein expression. Our results show that APLP2-CTFs upregulate S100A9 protein and mRNA expression in BV2 cells, and identify a novel pathway involved in neuronal injury and apoptosis, and repair and protection in Alzheimer's disease.
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Registered trials
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