ArticleNeurochemical research2022
Increase in Cellular Lysophosphatidylserine Content Exacerbates Inflammatory Responses in LPS-Activated Microglia.
Article in Neurochemical research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed, 7 citations in OpenAlex.
- Association ofInternational journal of molecular sciences · 2026Article
- A Novel Compound Heterozygous Variant in the ABHD12 Gene Cause PHARC Syndrome in a Chinese Family: The Proband Presenting New Genotype and Phenotype.Molecular genetics & genomic medicine · 2025Article
- PHARC syndrome: an overview.Orphanet journal of rare diseases · 2024Review
- Genotype-phenotype spectrum and correlation of PHARC Syndrome due to pathogenic ABHD12 variants.BMC medical genomics · 2024Article
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 2 institutions in 1 country.
Funding
Abstract
Mutations in alpha/beta-hydrolase domain containing (ABHD) 12 gene, which encodes lysophosphatidylserine (LysoPS) lipase, cause the neurodegenerative disease PHARC (Polyneuropathy, Hearing loss, Ataxia, Retinitis pigmentosa, Cataract). Since ABHD12 is expressed by microglia in the central nervous system and is localized to the endoplasmic reticulum, accumulation of intracellular LysoPS by ABHD12 mutations is assumed to be one of the pathological mechanisms associated with microglial activation in PHARC. However, the role of microglia in the PHARC brain and the relationship between microglial function and cellular LysoPS content remains unclear. Therefore, we explored the influence of cellular LysoPS content in microglial inflammatory responses. We evaluated the effects of inhibitors of cellular LysoPS metabolism, KC01 and DO-264, on inflammatory responses using a lipopolysaccharide (LPS)-stimulated mouse microglial cell line, BV-2 and primary microglia. Treatment of DO-264, an inhibitor of cellular LysoPS degradation, enhanced LPS-induced phagocytosis concomitant with the increase in cellular LysoPS content in BV-2 cells. On the other hand, treatment with KC01, an agent had been developed as an inhibitor of LysoPS synthase, reduced phagocytosis without affecting cellular LysoPS content. Such effects of both inhibitors on phagocytosis were also confirmed using primary microglia. KC01 treatment decreased nitric oxide (NO) production, accompanied by a reduction in inducible NO synthase expression in BV-2 microglia. KC01 also suppressed LPS-induced generation of intracellular reactive oxygen species and cytokines such as interleukin-6. Our results suggest that increase in cellular LysoPS levels can exacerbate microglial inflammatory responses. Treatment to prevent the increase in cellular LysoPS in microglia may have therapeutic potential for PHARC.
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.