STAT1‐avtiviated LINC00961 regulates myocardial infarction by the PI3K/AKT/GSK3β signaling pathway

Liu, Shengzhong; He, Ying; Shi, Jun; Liu, Lulu; Ma, Hao; Guo, Yingqiang

doi:10.1002/jcb.28596

Cited by 16 publications

(19 citation statements)

References 36 publications

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“…The control cells were cultured under normal conditions. After 24 h of culture, the following tests were carried out (24,25).…”

Section: Establishment Of Hypoxia Model Of Cardiomyocytesmentioning

confidence: 99%

RETRACTED: Silencing CircHIPK3 Sponges miR-93-5p to Inhibit the Activation of Rac1/PI3K/AKT Pathway and Improves Myocardial Infarction-Induced Cardiac Dysfunction

Yang

et al. 2021

Front. Cardiovasc. Med.

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The ceRNA network involving circular RNAs (circRNAs) is essential in the cardiovascular system. We investigated the underlying ceRNA network involving circHIPK3 in myocardial infarction (MI). After an MI model was established, cardiac function was verified, and myocardial tissue damage in mice with MI was evaluated. A hypoxia model of cardiomyocytes was used to simulate MI in vivo, and the expression of and targeting relationships among circHIPK3, miR-93-5p, and Rac1 were verified. The apoptosis of cardiomyocyte was identified. Gain- and loss-of-functions were performed to verify the ceRNA mechanism. The MI-modeled mice showed cardiac dysfunction and enlarged infarct size. CircHIPK3 was highly expressed in mouse and cell models of MI. Silencing circHIPK3 reduced infarct size, myocardial collagen deposition, and myocardial apoptosis rate and improved cardiac function. CircHIPK3 sponged miR-93-5p, and miR-93-5p targeted Rac1. Overexpression of miR-93-5p inhibited MI-induced cardiomyocyte injury and eliminated the harmful effect of circHIPK3. CircHIPK3 acted as ceRNA to absorb miR-93-5p, thus promoting the activation of the Rac1/PI3K/AKT pathway. We highlighted that silencing circHIPK3 can upregulate miR-93-5p and then inhibit the activation of Rac1/PI3K/Akt pathway, which can improve MI-induced cardiac dysfunction.

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“…The control cells were cultured under normal conditions. After 24 h of culture, the following tests were carried out (24,25).…”

Section: Establishment Of Hypoxia Model Of Cardiomyocytesmentioning

confidence: 99%

RETRACTED: Silencing CircHIPK3 Sponges miR-93-5p to Inhibit the Activation of Rac1/PI3K/AKT Pathway and Improves Myocardial Infarction-Induced Cardiac Dysfunction

Yang

et al. 2021

Front. Cardiovasc. Med.

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“…Studies have also shown a significant elevation of STAT1 expression in hypoxia-induced cardiomyocytes, and STAT1 knockout relieved cardiac damage MI mice [24,25]. Therefore, the dysregulation of IFIT3 expression in the myocardial tissues of mice with MI may be regulated by transcription factors, such as NF-κB p65, or interacting proteins, such as STAT1.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of interferon-induced protein with tetratricopeptide repeats 3 relieves the inflammatory response and myocardial fibrosis of mice with myocardial infarction and improves their cardiac function

et al. 2021

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Myocardial infarction (MI) is a common cardiovascular disease with high morbidity and mortality. In this study, we explored the role of interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) in MI. MI was induced by ligation of the left anterior descending coronary artery. Lentivirus-mediated RNA interference of IFIT3 expression was performed by tail vein injection 72 hours before MI modeling.Cardiac injury indexes and inflammatory response were examined 3 days after MI.Cardiac function indexes, infarct size, and cardiac fibrosis were assessed 4 weeks after MI. IFIT3 expression was upregulated in myocardial tissues at both 3 days and 4 weeks after MI. Knockdown of IFIT3 significantly relieved the myocardial injury, as evidenced by the decrease in serum levels of cTnI and CK-MB. In addition, IFIT3 knockdown significantly reduced the number of CD68 + macrophages and the levels of interleukin-1β, interleukin-6, and tumor necrosis factor-α, indicating that the inflammatory response was relieved. Moreover, IFIT3 silencing also significantly improved cardiac function and reduced infarct size, myocardial fibrosis, and collagen content in mice with MI. Mechanically, the present study showed that the activation of the MAPK pathway was observed in myocardial tissues of MI mice, which was blocked by IFIT3 knockdown, as indicated by the decreased phosphorylation of JNK, p-38, and ERK. Collectively, our results revealed the role of IFIT3 in the inflammatory response and myocardial fibrosis after MI, indicating that IFIT3 might be a potential target for MI treatment.

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“…In this study, miR-144-3p was observed to target at PTEN ’s 3′UTR and repress its expression at mRNA and protein levels (Figure 4). Previous studies have recommended that PTEN suppresses the activation of PI3K-Akt signaling pathway (Maehama, 2006; Bassi and Mak, 2016) which has been suggested to accelerate MI (Liu S. et al, 2019) and regulated myocardial infarct size and fibrosis (Wang et al, 2019). Moreover, PTEN is reported to be down-regulated in myocardial tissue during the process of myocardial fibrosis after MI in rats (Zhang and Cui, 2018).…”

Section: Discussionmentioning

confidence: 99%

MiR-144-3p Enhances Cardiac Fibrosis After Myocardial Infarction by Targeting PTEN

Yuan

Pan

Wen

et al. 2019

Front. Cell Dev. Biol.

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Myocardial infarction (MI) may cause heart failure and seriously harm human health. During the genesis of cardiac fibrosis after MI, the proliferation and migration of cardiac fibroblasts contribute to secretion and maintenance of extracellular matrix (ECM) components. Many miRNAs have been highly implicated in the processes of cardiac fibrosis after MI. However, the molecular mechanisms for how miRNAs involve in cardiac fibrosis remain largely unexplored. Based on MI model in miniature pigs, the potential miRNAs involved in MI were identified by using small RNA sequencing. Using human cardiac fibroblasts (HCFs) as a cellular model, EdU, Transwell, and the expression of ECM-related proteins were applied to investigate the cell proliferation, migration and collagen synthesis. In this study, using MI model based on miniature pigs, 84 miRNAs were identified as the differentially expressed miRNAs between MI and control group, and miR-144-3p, one of differentially expressed miRNAs, was identified to be higher expressed in infarct area. The cell proliferation, migration activity, and the mRNA and protein levels of the ECM-related genes were significantly increased by miR-144-3p mimic but significantly decreased by miR-144-3p inhibitor in cardiac fibroblasts. Furthermore, miR-144-3p was observed to repress transcription and translation of PTEN, and interfering with the expression of PTEN up-regulated the mRNAs and proteins levels of α-SMA, Col1A1, and Col3A1, and promoted the proliferation and migration of cardiac fibroblasts, which was in line with that of miR-144-3p mimics, but this observation could be reversed by miR-144-3p inhibitor. Collectively, miR-144-3p promotes cell proliferation, migration, and collagen production by targeting PTEN in cardiac fibroblasts, suggesting that miR-144-3p-mediated-PTEN regulation might be a novel therapeutic target for cardiac fibrosis after MI.

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STAT1‐avtiviated LINC00961 regulates myocardial infarction by the PI3K/AKT/GSK3β signaling pathway

Cited by 16 publications

References 36 publications

RETRACTED: Silencing CircHIPK3 Sponges miR-93-5p to Inhibit the Activation of Rac1/PI3K/AKT Pathway and Improves Myocardial Infarction-Induced Cardiac Dysfunction

RETRACTED: Silencing CircHIPK3 Sponges miR-93-5p to Inhibit the Activation of Rac1/PI3K/AKT Pathway and Improves Myocardial Infarction-Induced Cardiac Dysfunction

Downregulation of interferon-induced protein with tetratricopeptide repeats 3 relieves the inflammatory response and myocardial fibrosis of mice with myocardial infarction and improves their cardiac function

MiR-144-3p Enhances Cardiac Fibrosis After Myocardial Infarction by Targeting PTEN

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