Long Noncoding RNA Taurine-Upregulated Gene 1 Knockdown Protects Cardiomyocytes Against Hypoxia/Reoxygenation-induced Injury Through Regulating miR-532-5p/Sox8 Axis

Cai, Xinyong; Wang, Shu; Liu, Hong; Yu, Songping; Li, Bin; Zeng, Hong; Xu, Yang; Zhang, Ping; Shao, Liang

doi:10.1097/fjc.0000000000000895

Cited by 11 publications

(10 citation statements)

References 26 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Hu et al identified an oncogenic circASAP1 through circRNA sequencing in patients with HCC, which was proved to be associated with cancer initiation and metastasis via miR-326/miR-532-5p-MAPK1/CSF-1 signaling, respectively [ 90 ]. The result suggested that the underlying mechanism was also modulated by OS [ 91 , 92 ].…”

Section: The Mechanisms Of Ros-ncrnas Axis In Cancer Progressionmentioning

confidence: 99%

The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role

Zuo

Zhang

et al. 2022

Mol Cancer

View full text Add to dashboard Cite

Oxidative stress (OS), characterized by the excessive accumulation of reactive oxygen species (ROS), is an emerging hallmark of cancer. Tumorigenesis and development driven by ROS require an aberrant redox homeostasis, that activates onco-signaling and avoids ROS-induced programmed death by orchestrating antioxidant systems. These processes are revealed to closely associate with noncoding RNAs (ncRNAs). On the basis of the available evidence, ncRNAs have been widely identified as multifarious modulators with the involvement of several key redox sensing pathways, such as NF-κB and Nrf2 signaling, therefore potentially becoming effective targets for cancer therapy. Furthermore, the vast majority of ncRNAs with property of easy detected in fluid samples (e.g., blood and urine) facilitate clinicians to monitor redox homeostasis, indicating a novel method for cancer diagnosis. Herein, focusing on carcinoma initiation, metastasis and chemoradiotherapy resistance, we aimed to discuss the ncRNAs-ROS network involved in cancer progression, and the potential clinical application as biomarkers and therapeutic targets.

show abstract

Section: The Mechanisms Of Ros-ncrnas Axis In Cancer Progressionmentioning

confidence: 99%

The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role

Zuo

Zhang

et al. 2022

Mol Cancer

View full text Add to dashboard Cite

show abstract

“…In addition, miR-532-5p expression is downregulated in LPS-induced inflammation of RAW264.7 macrophages ( 23 ). It has been revealed that miR-532-5p serves an important role in the inflammatory response ( 24 ), oxidative stress ( 25 ) and apoptosis ( 8 ). However, to the best of our knowledge, the role of miR-532-5p in diabetes has not yet been reported.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‑532‑5p regulates oxidative stress and insulin secretion damage in high glucose‑induced pancreatic β cells by downregulating the expression levels of CCND1

Zhong¹,

Su²,

Chen

2021

Mol Med Rep

View full text Add to dashboard Cite

Diabetes mellitus is a metabolic disorder caused by insufficient insulin secretion. The expression of microRNA (miR)-532-5P is downregulated in diabetes, but its specific role in diabetes has not yet been elucidated. The present study aimed to investigate the specific mechanism underlying the effects of miR-532-5p on diabetes. Cell viability was determined using an MTT assay. The expression levels of miR-532-5P, cyclin D1 (CCND1), Insulin1 and Insulin2 were detected using reverse transcription-quantitative PCR. The expression of miR-532-5p and CCND1 were overexpressed in cells by cell transfection. ELISA was used to detect insulin secretion. 2′,7′-dichlorodihydrofluorescein diacetate was used to quantify reactive oxygen species levels in cells. Apoptosis was detected using a TUNEL assay. Western blotting was performed to detect the expression of apoptosis-related proteins, CCND1 and p53. A dual-luciferase reporter assay was conducted, and verified the targeted binding of miR-532-5p and CCND1. The expression of miR-532-5p was downregulated in high glucose (HG)-induced MIN6 cells. Overexpression of miR-532-5p could improve the HG-induced decline in insulin secretion and inhibit HG-induced oxidative stress and apoptosis in cells. miR-532-5p can target and regulate the expression of CCND1. Overexpression of miR-532-5p downregulated HG-induced cell insulin secretion, oxidative stress and apoptosis by downregulating CCND1, which is involved in regulating the expression of p53. To conclude, miR-532-5p regulated oxidative stress and insulin secretion damage in HG-induced pancreatic β cells by downregulating the expression of CCND1, which is involved in the upregulation of the expression of p53.

show abstract

“…The ChemiDoc XRS Imaging System (BioRad) was used to detect and quantify the specific protein. Grayscale determination was performed and statistical analysis using Fiji 40 …”

Section: Methodsmentioning

confidence: 99%

“…The gene expression was normalized to that of GAPDH using the 2 C t ∆∆ method. 39 Primers used for the research are as follows:…”

Section: Quantitative Real-time Polymerase Chain Reactionmentioning

confidence: 99%

MicroRNA‐582‐5p targeting Creb1 modulates apoptosis in cardiomyocytes hypoxia/reperfusion‐induced injury

Niu

Wang

Yang

et al. 2022

Immunity Inflam & Disease

View full text Add to dashboard Cite

Background Myocardial ischemia–reperfusion injury (MIRI) caused by the reperfusion therapy of myocardial ischemic diseases is a kind of major disease that threatens human health and lives severely. There are lacking of effective therapeutic measures for MIRI. MicroRNAs (miRNAs) are abundant in mammalian species and play a critical role in the initiation, promotion, and progression of MIRI. However, the biological role and molecular mechanism of miRNAs in MIRI are not entirely clear. Methods We used bioinformatics analysis to uncover the significantly different miRNA by analyzing transcriptome sequencing data from myocardial tissue in the mouse MIRI model. Multiple miRNA‐related databases, including miRdb, PicTar, and TargetScan were used to forecast the downstream target genes of the differentially expressed miRNA. Then, the experimental models, including male C57BL/6J mice and HL‐1 cell line, were used for subsequent experiments including quantitative real‐time polymerase chain reaction analysis, western blot analysis, hematoxylin and eosin staining, flow cytometry, luciferase assay, gene interference, and overexpression. Results MiR‐582‐5p was found to be differentially upregulated from the transcriptome sequencing data. The elevated levels of miR‐582‐5p were verified in MIRI mice and hypoxia/reperfusion (H/R)‐induced HL‐1 cells. Functional experiments revealed that miR‐582‐5p promoted apoptosis of H/R‐induced HL‐1 cells via downregulating cAMP‐response element‐binding protein 1 (Creb1). The inhibiting action of miR‐582‐5p inhibitor on H/R‐induced apoptosis was partially reversed after Creb1 interference. Conclusions Collectively, the research findings reported that upregulation of miR‐582‐5p promoted H/R‐induced cardiomyocyte apoptosis by inhibiting Creb1. The potential diagnostic and therapeutic strategies targeting miR‐582‐5p and Creb1 could be beneficial for the MIRI treatment.

show abstract

Long Noncoding RNA Taurine-Upregulated Gene 1 Knockdown Protects Cardiomyocytes Against Hypoxia/Reoxygenation-induced Injury Through Regulating miR-532-5p/Sox8 Axis

Cited by 11 publications

References 26 publications

The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role

The crosstalk between reactive oxygen species and noncoding RNAs: from cancer code to drug role

MicroRNA‑532‑5p regulates oxidative stress and insulin secretion damage in high glucose‑induced pancreatic β cells by downregulating the expression levels of CCND1

MicroRNA‐582‐5p targeting Creb1 modulates apoptosis in cardiomyocytes hypoxia/reperfusion‐induced injury

Contact Info

Product

Resources

About