ArticleJournal of neuroscience research2026
miR-19a-3p and miR-19b-3p Promote Microglia Activation Associated With Neuroinflammation.
Article in Journal of neuroscience research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- A Pilot Investigation of Circulating miRNA Expression in Individuals Exposed to Aluminum and Welding Fumes.Current issues in molecular biology · 2025Article
- Radiation-Induced miRNAs Changes and cf mtDNA Level in Trauma Surgeons: Epigenetic and Molecular Biomarkers of X-ray Exposure.International journal of molecular sciences · 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
4 authors.
Funding
Abstract
Neuroinflammation, driven by microglia activation and the production of pro-inflammatory cytokines, has been implicated in several neurological diseases and neuropathic pain. MicroRNAs (miRNAs) have emerged as important regulators of neuroinflammatory processes. Prior studies identified elevated levels of circulating miR-19a and miR-19b in individuals living with chronic pain following spinal cord injury (SCI). In this study, we wanted to determine whether miR-19a and miR-19b have a direct effect on microglia activation, specifically pro-inflammatory activation, associated with neuroinflammation. Microglia were activated by inflammatory stimuli in the presence of miR-19a or miR-19b mimics, and assessed for the expression of cytokines, chemokines, and effector molecules. The results show that miR-19a or miR-19b mimics increased the expression of pro-inflammatory cytokines, chemokines, and effector molecules in microglia. The results also showed decreased expression of suppressor of cytokine signaling (SOCS) proteins, namely SOCS1 and SOCS3, in activated microglia with miR-19a and miR-19b mimics. Additionally, enhanced signaling through the NFκB and Jak pathways was observed with increased NFkB-p65 and JAK1 phosphorylation in the presence of miR-19a and miR-19b mimics. Further results show that miR-19a and miR-19b inhibitors reversed these effects on activated microglia. Overall, our results demonstrate that miR-19a or miR-19b increased the expression of pro-inflammatory cytokines, chemokines, and effector molecules in activated microglia. These results indicate that miR-19a and miR-19b can enhance microglia activation and associated inflammatory responses, which may have implications for conditions associated with neuroinflammation.
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Registered trials
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