MicroRNAs as Potential Markers for Advantageous Perfusion in a Preclinical Donation after Cardiac Death Animal Model of Oxygenated Hypothermic Machine Perfusion (HOPE)

Gómez-Dos-Santos, Victoria; Hevia-Palacios, V.; Ramos-Muñoz, Edurne; García‐Bermejo, Maria Laura; Rodríguez-Serrano, Esperanza Macarena; Saiz-González, A.; Rey-Sánchez, José Manuel Del; Burgos-Revilla, F.J.

doi:10.21926/obm.transplant.1802012

Cited by 5 publications

(4 citation statements)

References 26 publications

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“…MicroRNAs are key post‐transcriptional regulators of gene expressions . They can bind to the 3′UTRs of the target mRNAs and repress mRNAs translation . CircRNAs generally exhibit regulatory functions on gene expression through acting as microRNA sponge .…”

Section: Discussionmentioning

confidence: 99%

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Retracted: Circular RNA ANKRD36 attends to lipopolysaccharide‐aroused MRC‐5 cell injury via regulating microRNA‐31‐3p

2019

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Background Some circular RNAs (circRNAs) are reported to attend to the pathogenesis of pneumonia. This study tested the impact of circRNA ankyrin repeat domain 36 (circANKRD36) on human embryonic lung fibroblast MRC‐5 cell injury irritated by lipopolysaccharide (LPS). Methods After LPS irritation, viability, apoptosis, ROS, protein, and cytokines, along with circANKRD36 were tested by CCK‐8, Annexin V‐FITC, DCFH‐DA, and ELISA or Western blot. si‐circANKRD36 and microRNA‐31‐3p/5p (miR‐31‐3p/5p) inhibitor were applied to silence circANKRD36 and miR‐31‐3p/5p. miR‐31‐3p/5p mimic was utilized to upregulate miR‐31‐3p/5p. RT‐qPCR was used to detect miRNAs. The relationship between miRNAs and MyD88 or IL‐34 was analyzed by luciferase activity reporter assay. Results LPS aroused a decrease in viability, increases in apoptosis, ROS, and IL‐6, IL‐8, and TNF‐α, along with circANKRD36, and activation of NF‐κB pathway. Silencing circANKRD36 weakened the above‐mentioned influences of LPS. Moreover, silencing circANKRD36 hoisted miR‐31‐3p expression. Silencing miR‐31‐3p mitigated the impacts of circANKRD36 silence on LPS‐irritated MRC‐5 cells. Besides, MyD88 was a downstream target of miR‐31‐3p, and 3′UTR of IL‐34 mRNA was targeted by miR‐31‐5p. LPS induced the accumulation of MyD88. Silencing MyD88 was constructive to maintain cell viability, retard apoptosis and inhibit adverse oxidation and inflammation. Conclusion This research verified that silencing circANKRD36 could weaken LPS‐irritated MRC‐5 cell injury via regulating miR‐31/MyD88‐mediated repression of NF‐κB pathway.

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Section: Discussionmentioning

confidence: 99%

“…29 They can bind to the 3 0 UTRs of the target mRNAs and repress mRNAs translation. 29,30 CircRNAs generally exhibit regulatory functions on gene expression through acting as microRNA sponge. 15,31 miR-31 are reported to present pro-inflammatory or antiinflammatory activities under different condition.…”

Section: R E T R a C T E Dmentioning

confidence: 99%

Retracted: Circular RNA ANKRD36 attends to lipopolysaccharide‐aroused MRC‐5 cell injury via regulating microRNA‐31‐3p

2019

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“…miRNAs are considered as the potential markers of advantageous perfusion [15]. Recent studies discovered that miR-29 is a key regulator in the pathophysiological process of fibrosis in kidney [16], lung [17], liver [18], as well as heart [19] through modulating collagen expression in these organs.…”

Section: Introductionmentioning

confidence: 99%

RETRACTED ARTICLE: Hypoxia-induced apoptosis of cardiomyocytes is restricted by ginkgolide B-downregulated microRNA-29

Ren

et al. 2020

Cell Cycle

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Ginkgolide B exerts a cardioprotective function against ischemia-caused apoptosis in myocardial infarction. Here we sought out to address a functional mechanism associated with microRNA-29 (miR-29). Rat cardiomyocytes (H9c2 cells) were cultured in ginkgolide B-conditioned medium prior to hypoxic induction. To construct miR-29-overexpressed cells, miR-29 mimic was transfected into H9c2 cells. The cells were harvested for assaying survivability and apoptosis by CCK-8 and FITC-Annexin V staining methods. Western blot was applied to identify apoptotic hallmarks and signaling transducers. RT-PCR was carried out for investigating miR-29 expression. Cardiomyocytes were sensitive to hypoxic apoptosis, while ginkgolide B intensified the abilities of cardiomyocytes to resist hypoxia by increasing survivability and repressing apoptosis. Specifically, ginkgolide B repressed Bax and cleaved caspase 3 while enhanced Bcl-2. Ginkgolide B buffered the expression of miR-29 induced by hypoxia. However, ginkgolide B showed a slight role in survivability and apoptosis in the cells overexpressing miR-29. Meanwhile, ginkgolide B triggered the phosphorylation of PI3 K and AKT, as well as induced Sp1, while this beneficial role was abrogated in the cells treated by miR-29 mimic. Our results confirmed that ginkgolide B might have therapeutic significance by repressing hypoxic apoptosis. Ginkgolide B-elicited miR-29 inhibition might be the basis of this beneficial role.

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“…MiRNAs are small (~ 22 nt) endogenous ncRNAs and involved in cell proliferation, survival, etc [12,13]. It has been reported that lncRNAs could interact with miRNA to regulate tumorigenesis and play key roles in the treatment and diagnosis for patients [14].…”

Section: Agingmentioning

confidence: 99%

Long non-coding RNA NNT-AS1 promotes cholangiocarcinoma cells proliferation and epithelial-to-mesenchymal transition through down-regulating miR-203

Zhu

Hui

et al. 2020

Aging

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Background: Cholangiocarcinoma (CCA) is a serious malignant tumor. Long non-coding RNA NNT-AS1 (NNT-AS1) takes crucial roles in several tumors. So, we planned to research the roles and underlying mechanism of NNT-AS1 in CCA. Results: NNT-AS1 overexpression was appeared in CCA tissues and cell lines. Proliferation was promoted by NNT-AS1 overexpression in CCLP1 and TFK1 cells. Besides, NNT-AS1 overexpression reduced E-cadherin level and raised levels of N-cadherin, vimentin, Snail and Slug. However, the opposite trend was occurred by NNT-AS1 knockdown. Further, NNT-AS1 overexpression promoted phosphatidylinositol 3 kinase (PI3K)/AKT and extracellular signal-regulated kinase (ERK)1/2 pathways. MiR-203 was sponged by NNT-AS1 and miR-203 mimic reversed the above promoting effects of NNT-AS1. Additionally, insulin-like growth factor type 1 receptor (IGF1R) and zinc finger E-box binding homeobox 1 (ZEB1) were two potential targets of miR-203. Conclusion: NNT-AS1 promoted proliferation, EMT and PI3K/AKT and ERK1/2 pathways in CCLP1 and TFK1 cells through down-regulating miR-203. Methods: CCLP1 and TFK1 cells were co-transfected with pcDNA-NNT-AS1 and miR-203 mimic. Bromodeoxyuridine (BrdU), flow cytometry, quantitative reverse transcription polymerase chain reaction (qRT-PCR) and western blot were employed to detect roles and mechanism of NNT-AS1. Interaction between NNT-AS1 and miR-203 or miR-203 and target genes was examined through luciferase activity experiment.

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MicroRNAs as Potential Markers for Advantageous Perfusion in a Preclinical Donation after Cardiac Death Animal Model of Oxygenated Hypothermic Machine Perfusion (HOPE)

Abstract: Background: Extended criteria donors and donations after cardiac death provide organs that tend to be more sensitive to the stresses of preservation. The potential role of oxygen in preservation techniques remains to be clarified. The aim of this study was to compare

Cited by 5 publications

References 26 publications

Retracted: Circular RNA ANKRD36 attends to lipopolysaccharide‐aroused MRC‐5 cell injury via regulating microRNA‐31‐3p

Retracted: Circular RNA ANKRD36 attends to lipopolysaccharide‐aroused MRC‐5 cell injury via regulating microRNA‐31‐3p

RETRACTED ARTICLE: Hypoxia-induced apoptosis of cardiomyocytes is restricted by ginkgolide B-downregulated microRNA-29

Long non-coding RNA NNT-AS1 promotes cholangiocarcinoma cells proliferation and epithelial-to-mesenchymal transition through down-regulating miR-203

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