ArticleCell biochemistry and biophysics2025
miR-634 Mediated Aquaporin 5 Expression Regulates the Inflammatory Response and Apoptosis in Lipopolysaccharide-Induced Human Nasal Epithelial Cells.
Article in Cell biochemistry and biophysics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
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
1 citing paper in PubMed.
- Clinical Significance and Mechanistic Role of circLPAR3/miR-634 in Ischemic Stroke.Neurochemical research · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To investigate the effects and potential mechanism of miR-634 that regulates aquaporin 5 (AQP5) to regulate the inflammatory response and apoptosis in LPS-induced human nasal epithelial cells (HNEpCs). The mRNA expressions of miR-634 and AQP5 in the tissues of patients with chronic rhinosinusitis (CRS) and LPS-induced HNEpCs were detected by qRT-PCR. Western blotting was performed to detect the protein expression of AQP5 in HNEpCs. The apoptosis was assessed by flow cytometry. The cell viability was detected by CCK-8 kit. Combined with bioinformatics analysis, dual-luciferase reporter and western blotting, the interaction between AQP5 and miR-634 were predicted and verified. It proved that the mRNA expression of miR-634 in CRS group was significantly up-regulated, while AQP5 was down-regulated. And the expression of AQP5 in CRS group was down-regulated compared with control group. In vitro experiments indicated that the expression of miR-634 increased gradually, while AQP5 decreased gradually with the increase of LPS concentration. The cell viability was inhibited and apoptosis was promoted in LPS-induced group. In addition, it was found that miR-634 could inhibit cell viability and promote apoptosis. QRT-PCR results implied that miR-634 up-regulated the expression of inflammatory factor-related mRNA in LPS-induced HNEpCs. Combined with bioinformatics analysis and qRT-PCR, it was confirmed that AQP5 was the direct target of miR-634. MiR-634 directly targeted AQP5 to regulate CRS progression, including inhibiting cell viability, promoting apoptosis and aggravating inflammatory response, which may provide theoretical basis for its use as a biomarker for CRS treatment.
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Identifiers
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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.