ArticleRSC advances2019
Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages.
Article in RSC advances, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. 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, 4 citations in OpenAlex.
- An overview of natural products that modulate the expression of non-coding RNAs involved in oxidative stress and inflammation-associated disorders.Frontiers in pharmacology · 2023Review
- LncRNA OIP5‑AS1 aggravates house dust mite‑induced inflammatory responses in human bronchial epithelial cells via the miR‑143‑3p/HMGB1 axis.Molecular medicine reports · 2020Article
Corrections and comments
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA OIP5-AS1 (lncRNA OIP5-AS1) and microRNA-128-3p (miRNA-128-3p) have been reported to play significant roles in human diseases. However, their role in atherosclerosis (AS) has been less studied. The aim of this research was to reveal the roles and functional mechanisms of OIP5-AS1 and miRNA-128-3p in AS development. Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assays were performed to detect gene expression. Cell proliferation and apoptosis were assessed using a 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry analysis, respectively. In addition, ELISA was employed to determine the levels of interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α. Oxidative stress was examined using a relevant kit. Furthermore, the interaction between miR-128-3p and OIP5-AS1 or cyclin-dependent kinase inhibitor 2A (CDKN2A) was predicted using StarBase, and then confirmed using the dual-luciferase reporter assay or the RNA immunoprecipitation (RIP) assay. We found that OIP5-AS1 and CDKN2A levels were upregulated and the miR-128-3p level was downregulated in oxidized low-density lipoprotein (ox-LDL)-induced THP1 cells. OIP5-AS1 knockdown weakened the regulatory effect of ox-LDL on cell progression. Interestingly, OIP5-AS1 directly interacted with miR-128-3p and miR-128-3p-targeted CDKN2A. Furthermore, OIP5-AS1 regulated ox-LDL-induced cell progression through modulating miR-128-3p expression, and miR-128-3p exerted its influence by modulating the CDKN2A level. Finally, we confirmed that OIP5-AS1 suppressed miR-128-3p expression to increase the level of CDKN2A. In conclusion, our findings demonstrate that OIP5-AS1 knockdown repressed the effect of ox-LDL on cell progression through regulating the miR-128-3p/CDKN2A axis, providing a potential target for the treatment of 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.