ArticleRSC advances2019
Retracted Article: Knockdown of long non-coding RNA OIP5-AS1 suppresses cell proliferation and migration in ox-LDL-induced human vascular smooth muscle cells (hVMSCs) through targeting miR-152-3p/PAPPA axis.
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 It has been retracted, and should not be counted.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, 2 citations in OpenAlex.
- LncRNA XIST regulates atherosclerosis progression in ox-LDL-induced HUVECs.Open medicine (Warsaw, Poland) · 2021Article
- lncRNA Oip5-as1 attenuates myocardial ischaemia/reperfusion injury by sponging miR-29a to activate the SIRT1/AMPK/PGC1α pathway.Cell proliferation · 2020Article
Corrections and comments
- Retracted
Authors and funding
6 authors at 2 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Emerging evidence has demonstrated that long non-coding RNA Opa-interacting protein 5 antisense RNA 1 (OIP5-AS1) is associated with cellular behaviors among malignant tumors. However, the role of OIP5-AS1 in atherosclerosis remains largely undefined. The aim of this study was to explore the expression and role of OIP5-AS1 in a cell model of atherosclerosis, as well as the underlying mechanism. We found that expression of OIP5-AS1 was upregulated in human vascular smooth muscle cells (hVMSCs) under oxidized low density lipoprotein (ox-LDL) administration, and knockdown of OIP5-AS1 suppressed cell viability (CCK-8) and proliferating cell nuclear antigen (PCNA) protein level in ox-LDL-treated hVMSCs, as well as inhibited cell migration rate (wound healing assay) and protein expression of matrix metalloproteinase (MMP)-2 and MMP-9. Mechanically, OIP5-AS1 functioned as competing endogenous RNA (ceRNA) to positively regulate PAPPA expression through sponging miRNA-152-3p (miR-152), and pregnancy-associated plasma protein A (PAPPA) was identified as a downstream target gene for miR-152. Moreover, expression of miR-152 was downregulated and PAPPA was upregulated in ox-LDL-treated hVMSCs. Similarly to OIP5-AS1 knockdown, miR-215 overexpression could inhibit cell proliferation and migration of hVMSCs administrated by ox-LDL, which was abated by PAPPA upregulation. Moreover, miR-215 downregulation partially reversed the suppressive role of OIP5-AS1 knockdown as well. In conclusion, knockdown of OIP5-AS1 suppressed ox-LDL-treated hVMSC proliferation and migration presumably through targeting miR-152/PAPPA axis, suggesting a novel OIP5-AS1/miR-152/PAPPA pathway in atherogenesis.
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.