ArticleJournal of neural transmission (Vienna, Austria : 1996)2015
Lipopolysaccharide treatment arrests the cell cycle of BV-2 microglial cells in G₁ phase and protects them from UV light-induced apoptosis.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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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
6 citing papers in PubMed, 7 citations in OpenAlex.
- Optineurin Shapes Basal and LPS-Induced Transcriptomes in BV2 Microglia.International journal of molecular sciences · 2025Article
- Polarized microtubule remodeling transforms the morphology of reactive microglia and drives cytokine release.Nature communications · 2023Article
- Involvement of lncRNA-HOTTIP in the Repair of Ultraviolet Light-Induced DNA Damage in Spermatogenic Cells.Molecules and cells · 2019Article
- Article
- Magnesium Lithospermate B Suppresses Lipopolysaccharide-Induced Neuroinflammation in BV2 Microglial Cells and Attenuates Neurodegeneration in Lipopolysaccharide-Injected Mice.Journal of molecular neuroscience : MN · 2018Article
- Effects of lipopolysaccharide on maturation of bovine oocyte in vitro and its possible mechanisms.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We previously reported that an optimal dose of lipopolysaccharide (LPS) markedly extends the lifespan of murine primary-cultured microglia by suppressing cell death pathways. In this study, we investigated the effects of LPS pretreatment on UV light-induced apoptosis of cells from the microglial cell line BV-2. More than half of BV-2 cells were apoptotic, and procaspase-3 was cleaved into its active form at 3 h of UV irradiation. In contrast, in BV-2 cells treated with LPS for 24 h, UV irradiation caused neither apoptosis nor procaspase-3 cleavage. LPS treatment arrested the cell cycle in G1 phase and upregulated cyclin-dependent kinase inhibitor p21(Waf1/Cip1) and growth arrest and DNA damage-inducible (GADD) 45α in BV-2 cells. When p21(Waf1/Cip1) and GADD45α were knocked down by small interfering RNA, procaspase-3 was cleaved into its active form to induce apoptosis. Our findings suggest that LPS inhibits UV-induced apoptosis in BV-2 cells through arrest of the cell cycle in G1 phase by upregulation of p21(Waf1/Cip1) and GADD45α. Excessive activation of microglia may play a critical role in the exacerbation of neurodegeneration, therefore, normalizing the precise regulation of apoptosis may be a new strategy to prevent the deterioration caused by neurodegenerative disorders.
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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.