LncRNA KCNQ1OT1 as a miR-26a-5p sponge regulates ATG12-mediated cardiomyocyte autophagy and aggravates myocardial infarction

Li, Jinbei; Tong, Yalin; Zhou, Yanjun; Han, Zhanying; Wang, Xule; Ding, Tongbin; Qu, Yongsheng; Zhang, Zhiliang; Chang, Chao; Zhang, Xiaoli; Qiu, Chunguang

doi:10.1016/j.ijcard.2021.05.053

Cited by 19 publications

(6 citation statements)

References 30 publications

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“…Mounting evidence manifested that lncRNA KCNQ1OT1 participated in regulating cell progression and differentiation among various diseases such as cancer, fracture, and myocardial infarction (Feng et al, 2020;Wang et al, 2020;Li et al, 2021b;Hong et al, 2021). According to the previous study, KCNQ1OT1 was upregulated in the ischemic brain tissue, and its expression was growing with the patients' severity of neurological impairments.…”

Section: Discussionmentioning

confidence: 99%

LncRNA KCNQ1OT1 predicts further cerebral events in patients with transient ischemic attack

J²,

Sun³

et al. 2022

Front. Pharmacol.

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Transient ischemic attack (TIA) poses a great threat of cerebrovascular diseases to a large number of patients, despite its reversible neurological dysfunction. Long non-coding RNAs (lncRNAs) have been proven to play critical roles in the pathophysiological development of cerebrovascular events. Exploring the function of lncRNAs in modulating TIA prognosis would help to develop individualized therapeutics. A total of 231 participants with the first onset of TIA were recruited in the study, including 65 subsequent stroke patients. The expression of lncRNA potassium voltage-gated channel subfamily Q member 1 opposite strand 1 (KCNQ1OT1) was upregulated in patients with recurrent ischemic events after TIA. Additionally, KCNQ1OT1 could be regarded as an independent predictor for subsequent ischemic stroke. The optimal diagnostic value was determined at 1.29 with a sensitivity of 63% and a specificity of 72%. Fewer patients would survive from further ischemic stroke with their KCNQ1OT1 level over 1.29. Furthermore, the expression of KCNQ1OT1 was elevated with a growing serum high-sensitivity C-reactive protein (hs-CRP) level. KCNQ1OT1 might be involved in the regulation of early inflammatory response during recurrence of TIA.

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Section: Discussionmentioning

confidence: 99%

LncRNA KCNQ1OT1 predicts further cerebral events in patients with transient ischemic attack

J²,

Sun³

et al. 2022

Front. Pharmacol.

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“…KCNQ1OT1 knockdown inhibited autophagy and protected cardiomyocytes from apoptosis by upregulating miR-26a-5p. [ 46 ] Recent studies suggest that XIST targets the corresponding miRNAs and regulates the pathological processes in MI. Silencing of XIST inhibited myocardial apoptosis in rats with MI by regulating miR-449.…”

Section: Discussionmentioning

confidence: 99%

Construction of LncRNA-mediated CeRNA network for investigating the immune pathogenesis of myocardial infarction

Wei,

Meng,

Fan

et al. 2024

Medicine

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Background: Myocardial infarction (MI) is a cardiovascular disease that seriously threatens human health. However, an immune-related competitive endogenous RNA (ceRNA) network has not been reported in MI. Methods: The GSE66360, GSE19339, GSE97320, GSE61741, and GSE168281 datasets were acquired from the Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) and differentially expressed miRNAs (DEmiRNAs) from MI patients and healthy controls were screened and an immune-related ceRNA network was constructed. Furthermore, the key long noncoding RNAs(lncRNAs) highly related to the immune mechanism of MI were identified utilizing the random walk with restart algorithm. Finally, the expression of the hub genes was further verified in the GSE66360, GSE19339, and GSE97320 datasets, and quantitative real-time polymerase chain reaction (qRT-PCR) was performed for the MI patients and healthy controls. Results: A total of 184 differentially expressed immune-related genes (DE-IRGs) and 432 DE-miRNAs were obtained, and an immune-related ceRNA network comprising 1421 lncRNAs, 61 DE-miRNAs, and 139 DE-IRGs was constructed. According to the order of stress, betweenness, and closeness, NEAT1, KCNQ1OT1, and XIST were identified as key lncRNAs. Moreover, random walk with restart analysis also suggested that NEAT1, KCNQ1OT1, and XIST are key lncRNAs. Subsequently, a ceRNA network of 10 hub genes and 3 lncRNAs was constructed. Finally, we found that the expression of FCER1G and TYROBP significantly differed between MI patients and control individuals in the GSE66360, GSE19339, and GSE97320 datasets. qRT–PCR revealed that the expression of NEAT1, KCNQ1OT1, XIST, FCER1G, and TYROBP was significantly elevated in MI tissue samples compared to healthy control tissue samples. Conclusion: NEAT1, KCNQ1OT1, XIST, FCER1G, and TYROBP are involved in MI and can be used as molecular biomarkers for the screening and diagnosis of MI. Furthermore, the immune system plays an essential role in the onset and progression of MI.

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“…It could protect against myocardial ischemia/reperfusion injury by regulating PTEN/PI3K/AKT signaling pathway 56 and also alleviates myocardial infarction by regulating ATG12‐mediated autophagy in cardiomyocytes. 57 In neurological diseases, miR‐26a‐5p could target DYRK1A to inhibits Tau phosphorylation and Aβ accumulation, which ameliorated the cognitive dysfunction, in Alzheimer's disease mice. 58 More importantly, miR‐26a‐5p presented favorable antiinflammatory effect in several disease model.…”

Section: Discussionmentioning

confidence: 99%

miR‐26a‐5p alleviates CFA‐induced chronic inflammatory hyperalgesia through Wnt5a/CaMKII/NFAT signaling in mice

Liu

Guo

et al. 2023

CNS Neurosci Ther

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Background: Inflammation often leads to the occurrence of chronic pain, and many miRNAs have been shown to play a key role in the development of inflammatory pain.However, whether miR-26a-5p relieves pain induced by inflammation and its possible mechanism are still unclear. Methods:The complete Freund's adjuvant (CFA)-induced inflammatory pain mouse model was employed. Intrathecal or subcutaneous injection of miR-26a-5p agomir was performed after modeling to study its antinociceptive effect and the comparison of different administration methods. Bioinformatics analysis of miRNAs was performed to study the downstream mechanisms of miR-26a-5p. HE staining, RT-qPCR, Western blotting, and immunofluorescence were used for further validation.Results: A single intrathecal and subcutaneous injection of miR-26a-5p both reversed mechanical hypersensitivity and thermal latency in the left hind paw of mice with CFA-induced inflammatory pain. HE staining and immunofluorescence studies found that both administrations of miR-26a-5p alleviated inflammation in the periphery and spinal cord. Bioinformatics analysis and dual-luciferase reporter gene analysis identified Wnt5a as a direct downstream target gene of miR-26a-5p. Wnt5a was mainly expressed in neurons and microglia in the spinal cord of mice with inflammatory pain.Intrathecal injection of miR-26a-5p could significantly reduce the expression level of Wnt5a and inhibit the downstream molecules of noncanonical Wnt signaling Camk2/ NFAT, inhibiting the release of spinal cord inflammatory factors and alleviating the activation of microglia. In addition, miR-26a-5p could also inhibit lipopolysaccharide (LPS)-stimulated BV2 cell inflammation in vitro through a noncanonical Wnt signaling pathway.Conclusions: miR-26a-5p is a promising therapy for CFA-induced inflammatory pain.Both intrathecal and subcutaneous injections provide relief for inflammatory pain. miR-26a-5p regulated noncanonical Wnt signaling to be involved in analgesia partly through antineuroinflammation, suggesting a pain-alleviating effect via noncanonical Wnt signaling pathway in the CFA-induced inflammatory pain model in vivo.

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LncRNA KCNQ1OT1 as a miR-26a-5p sponge regulates ATG12-mediated cardiomyocyte autophagy and aggravates myocardial infarction

Cited by 19 publications

References 30 publications

LncRNA KCNQ1OT1 predicts further cerebral events in patients with transient ischemic attack

LncRNA KCNQ1OT1 predicts further cerebral events in patients with transient ischemic attack

Construction of LncRNA-mediated CeRNA network for investigating the immune pathogenesis of myocardial infarction

miR‐26a‐5p alleviates CFA‐induced chronic inflammatory hyperalgesia through Wnt5a/CaMKII/NFAT signaling in mice

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