ArticleAmerican journal of translational research2022
Long non-coding RNA HOXA11-AS protects the barrier function of corneal endothelial cells by sponging microRNA-155 to alleviate corneal endothelial injury.
Article in American journal of translational research, 2022. 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.
The trial behind it
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- ELAVL1 promotes ferroptosis via the TRIM21/HOXD8 axis to inhibit osteogenic differentiation in congenital pseudoarticular tibia-derived mesenchymal stem cells.Journal of cell communication and signaling · 2025Article
- Global Transcriptome Analysis Reveals Distinct Phases of the Endothelial Response to TNF.Journal of immunology (Baltimore, Md. : 1950) · 2024Article
- Unveiling the Network regulatory mechanism of ncRNAs on the Ferroptosis Pathway: Implications for Preeclampsia.International journal of women's health · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesCorneal endothelial cells (CECs) are extremely vulnerable to injury. In this study, the role and mechanism of action of the long non-coding RNA HOXA11-AS during corneal endothelial injury (CEI) were evaluated in vivo and in vitro.
methodsScratch wounds were made to induce CEI in the corneal endothelium of rats and mice. Homeobox A11 (HOXA11)-AS expression was determined at different time points using quantitative real-time PCR. Human CECs with HOXA11-AS overexpression or downregulation were examined for survival, ferroptosis, and migration. Bioinformatics and dual-luciferase reporter assays were used to investigate the correlation between HOXA11-AS and microRNA (miR)-155.
resultsHOXA11-AS expression was reduced in the corneal endothelium in a time-dependent manner. Scratch wounds triggered high rates of ferroptosis and migration in CECs and impaired cell proliferation. HOXA11-AS overexpression partially attenuated the scratch wound-induced changes in proliferation, ferroptosis, and migration, whereas silencing HOXA11-AS had the opposite effects. Moreover, HOXA11-AS served as a competing endogenous RNA of miR-155. Levels of miR-155 were upregulated in the corneal endothelium following the scratch injury, and this upregulation abolished the effect of HOXA11-AS overexpression on the behavior of CECs after injury; miR-155 inhibition counteracted the effect of HOXA11-AS silencing.
conclusionsHOXA11-AS exerts protective effects against CEI by sponging miR-155, suggesting that these loci are treatment targets for corneal endothelial disorders.
Indexed as
Identifiers
36628203PMC9827337W4315619381What OpenQuestion holds
Registered trials
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