Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages

Li, Xiaojuan; Quansheng, Cao; Wang, Yanyu; Wang, Yongsheng

doi:10.1039/c9ra08322g

Cited by 4 publications

(3 citation statements)

References 36 publications

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“…in a recent study, oiP5-aS1 could promote apoptosis of bladder cancer cells (39). Besides, oiP5-aS1 could also facilitate ox-LDL-induced inflammation and oxidative stress in macrophages, as well as induce ox-ldl mediated vascular endothelial cells apoptosis (24,25). consistent with these previous findings, the present study demonstrated that oiP5-aS1 knockdown inhibited der p1-induced apoptosis.…”

Section: Discussionmentioning

confidence: 93%

“…other studies have also indicated that lncrnas TcF7 and GaS5 promote the development of asthma (22,23). among these lncrnas, lncrna opa-interacting protein 5 antisense rna1 (oiP5-aS1) was demonstrated to promote inflammation in several cell types, including macrophages and endothelial cells (24,25). Since inflammation is one of the pathological causes of asthma, it may be hypothesized that oiP5-aS1 could serve a functional role in bronchial asthma.…”

Section: Introductionmentioning

confidence: 98%

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LncRNA OIP5‑AS1 aggravates house dust mite‑induced inflammatory responses in human bronchial epithelial cells via the miR‑143‑3p/HMGB1 axis

et al. 2020

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Bronchial asthma poses a serious threat to human health. Previous studies have documented the role of long non-coding rnas (lncrnas) in asthma. However, the molecular mechanism underlying bronchial asthma remains unclear. The aim of the present study was to evaluate the role of the lncrna opa-interacting protein 5 antisense rna1 (oiP5-aS1) in the house dust mite-induced inflammatory response in human bronchial epithelial cells. BeaS-2B cells were treated with Dermatophagoides pteronyssinus peptidase 1 (der p1) to establish an in vitro model of asthma. oiP5-aS1 expression levels increased in BeaS-2B cells following der p1 treatment, while microrna (mir)-143-3p was downregulated. additionally, the levels of the pro-inflammatory factors tumor necrosis factor-α, interleukin (il)-6 and il-8 were measured, and apoptosis was evaluated following oiP5 silencing. oiP5-aS1 knockdown reduced the inflammatory response and apoptosis in BeaS-2B cells. Furthermore, using dual luciferase reporter assays and co-transfection experiments, it was demonstrated that the function of oiP5-aS1 was mediated by mir-143-3p. mir-143-3p overexpression attenuated the Der p1-induced inflammatory response and apoptosis of BeaS-2B cells by targeting high mobility group box 1 (HMGB1). in summary, oiP5-aS1 exacerbated Der p1-induced inflammation and apoptosis in BeaS-2B cells by targeting mir-143-3p via HMGB1.

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Section: Discussionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 98%

LncRNA OIP5‑AS1 aggravates house dust mite‑induced inflammatory responses in human bronchial epithelial cells via the miR‑143‑3p/HMGB1 axis

et al. 2020

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“…We also observed that some lncRNAs can regulate oxidative stress and inflammation at the same time. The lncRNA Linc00638 acts by activating the Nrf2/HO-1 signaling pathways following an increase in its level of expression to inhibit oxidative stress and inflammation in rheumatoid arthritis (Sun et al, 2021); lncRNA OIP5-AS1 promotes inflammation and oxidative stress via up modulation of miR-128-3P expression to inhibit cyclindependent kinase 2A (Li et al, 2019).…”

Section: Gingerolmentioning

confidence: 99%

An overview of natural products that modulate the expression of non-coding RNAs involved in oxidative stress and inflammation-associated disorders

et al. 2023

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Oxidative stress is a state in which oxidants are produced in excess in the body’s tissues and cells, resulting in a biological imbalance amid the generation of reactive oxygen and nitrogen species (RONS) from redox reactions. In case of insufficient antioxidants to balance, the immune system triggers signaling cascades to mount inflammatory responses. Oxidative stress can have deleterious effects on major macromolecules such as lipids, proteins, and nucleic acids, hence, Oxidative stress and inflammation are among the multiple factors contributing to the etiology of several disorders such as diabetes, cancers, and cardiovascular diseases. Non-coding RNAs (ncRNAs) which were once referred to as dark matter have been found to function as key regulators of gene expression through different mechanisms. They have dynamic roles in the onset and development of inflammatory and oxidative stress-related diseases, therefore, are potential targets for the control of those diseases. One way of controlling those diseases is through the use of natural products, a rich source of antioxidants that have drawn attention with several studies showing their involvement in combating chronic diseases given their enormous gains, low side effects, and toxicity. In this review, we highlighted the natural products that have been reported to target ncRNAs as mediators of their biological effects on oxidative stress and several inflammation-associated disorders. Those natural products include Baicalein, Tanshinone IIA, Geniposide, Carvacrol/Thymol, Triptolide, Oleacein, Curcumin, Resveratrol, Solarmargine, Allicin, aqueous extract or pulp of Açai, Quercetin, and Genistein. We also draw attention to some other compounds including Zanthoxylum bungeanum, Canna genus rhizome, Fuzi-ganjiang herb pair, Aronia melanocarpa, Peppermint, and Gingerol that are effective against oxidative stress and inflammation-related disorders, however, have no known effect on ncRNAs. Lastly, we touched on the many ncRNAs that were found to play a role in oxidative stress and inflammation-related disorders but have not yet been investigated as targets of a natural product. Shedding more light into these two last points of shadow will be of great interest in the valorization of natural compounds in the control and therapy of oxidative stress- and inflammation-associated disorders.

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Dysregulation of GAS5 and OIP5-AS1 lncRNAs in periodontitis

et al. 2020

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Retracted Article: LncRNA OIP5-AS1 contributes to ox-LDL-induced inflammation and oxidative stress through regulating the miR-128-3p/CDKN2A axis in macrophages

Abstract: Long non-coding RNA OIP5-AS1 (lncRNA OIP5-AS1) plays a significant role in ox-LDL induced inflammation.

Cited by 4 publications

References 36 publications

LncRNA OIP5‑AS1 aggravates house dust mite‑induced inflammatory responses in human bronchial epithelial cells via the miR‑143‑3p/HMGB1 axis

LncRNA OIP5‑AS1 aggravates house dust mite‑induced inflammatory responses in human bronchial epithelial cells via the miR‑143‑3p/HMGB1 axis

An overview of natural products that modulate the expression of non-coding RNAs involved in oxidative stress and inflammation-associated disorders

Dysregulation of GAS5 and OIP5-AS1 lncRNAs in periodontitis

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