Circ_0050908 up-regulates TRAF3 by sponging miR-324-5p to aggravate myocardial ischemia-reperfusion injury

Zhang, Qianrong; Cheng, Haijuan; Yang, Cuiling; Wang, Xinyan

doi:10.1016/j.intimp.2022.108740

Cited by 12 publications

(3 citation statements)

References 28 publications

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“…[62] In addition, TRAF3, which is regulated by the lncRNA Gm4419/miR-682 axis and circ_0050908/ miR-324-5p axis, exacerbates MI/RI. [63,64] In our study, we found that TRAF3 expression was apparently enhanced in rats with MI/RI.…”

Section: Discussionsupporting

confidence: 55%

ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis

Li,

Wang,

Tan

et al. 2024

J Biochem & Molecular Tox

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Myocardial ischemia‒reperfusion injury (MI/RI) is closely related to pyroptosis. alkB homolog 5 (ALKBH5) is abnormally expressed in the MI/RI models. However, the detailed molecular mechanism of ALKBH5 in MI/RI has not been elucidated. In this study, rats and H9C2 cells served as experimental subjects and received MI/R induction and H/R induction, respectively. The abundance of the targeted molecules was evaluated using RT‐qPCR, Western blotting, immunohistochemistry, immunofluorescence, and enzyme‐linked immunosorbent assay. The heart functions of the rats were evaluated using echocardiography, and heart injury was evaluated. Cell viability and pyroptosis were determined using cell counting Kit‐8 and flow cytometry, respectively. Total m6A modification was measured using a commercial kit, and pri‐miR‐199a‐5p m6A modification was detected by Me‐RNA immunoprecipitation (RIP) assay. The interactions among the molecules were validated using RIP and luciferase experiments. ALKBH5 was abnormally highly expressed in H/R‐induced H9C2 cells and MI/RI rats. ALKBH5 silencing improved injury and inhibited pyroptosis. ALKBH5 reduced pri‐miR‐199a‐5p m6A methylation to block miR‐199a‐5p maturation and inhibit its expression. TNF receptor‐associated Factor 3 (TRAF3) is a downstream gene of miR‐199a‐5p. Furthermore, in H/R‐induced H9C2 cells, the miR‐199a‐5p inhibitor‐mediated promotion of pyroptosis was reversed by ALKBH5 silencing, and the TRAF3 overexpression‐mediated promotion of pyroptosis was offset by miR‐199a‐5p upregulation. ALKBH5 silencing inhibited pri‐miR‐199a‐5p expression and enhanced pri‐miR‐199a‐5p m6A modification to promote miR‐199a‐5p maturation and enhance its expression, thereby suppressing pyroptosis to alleviate MI/RI through decreasing TRAF3 expression.

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Section: Discussionsupporting

confidence: 55%

ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis

Li,

Wang,

Tan

et al. 2024

J Biochem & Molecular Tox

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“…Through a literature search, we found that in addition to the miR‐138‐5p we studied, five more miRNAs (miR‐98‐5p, miR‐338‐5p, miR‐25‐3p, miR‐200a‐3p, miR‐324‐5p) were reported to have low expression during myocardial ischemia and reperfusion, and improving their expression can alleviate MIRI. MiR‐98‐5p exerted such function by reducing TLR4 and activating PI3K/AKT signal pathway, 27 miR‐338‐5p alleviated cerebral I/R injury through rapamycin pathway, 28 miR‐25‐3p alleviated myocardial infarction by targeting EZH2 and pro‐apoptotic proteins, 29 miR‐200a‐3p regulated MIRI by PDCD4 signal axis, 30 miR‐324‐5p regulated MIRI by TRAF3 and Mtfr1 signal 31,32 . Based on these notions and evidence, miR‐138‐5p could be one of the key targets of circHECTD1 during MIRI regulation and reflect a facet of the complex signal network of circHECTD1 in MIRI.…”

Section: Discussionmentioning

confidence: 93%

“…MiR-98-5p exerted such function by reducing TLR4 and activating PI3K/AKT signal pathway, 27 miR-338-5p alleviated cerebral I/R injury through rapamycin pathway, 28 miR-25-3p alleviated myocardial infarction by targeting EZH2 and pro-apoptotic proteins, 29 miR-200a-3p regulated MIRI by PDCD4 signal axis, 30 miR-324-5p regulated MIRI by TRAF3 and Mtfr1 signal. 31,32 Based on these notions and evidence, miR-138-5p could be one of the key targets of circHECTD1 during MIRI regulation and reflect a facet of the complex signal network of circHECTD1 in MIRI.…”

Section: Mir-138-5p Attenuated H/r-induced Myocardial Inflammatory Re...mentioning

confidence: 99%

CircHECTD1 promoted MIRI‐associated inflammation via inhibiting miR‐138‐5p and upregulating ROCK2

Yang

Luo

et al. 2023

The Kaohsiung J of Med Scie

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Myocardial ischemia–reperfusion injury (MIRI) was often observed after surgeries, causing a lot of suffering to patients. Inflammation and apoptosis were critical determinants during MIRI. We conveyed experiments to reveal the regulatory functions of circHECTD1 in MIRI development. The Rat MIRI model was established and determined by 2,3,5‐triphenyl tetrazolium chloride (TTC) staining. We analyzed cell apoptosis using TUNEL and flow cytometry. Proteins expression was evaluated by western blot. The RNA level was determined by qRT‐PCR. Secreted inflammatory factors were analyzed by ELISA assay. To predict the interaction sequences on circHECTD1, miR‐138‐5p, and ROCK2, bioinformatics analysis was performed. Dual‐luciferase assay was used to confirm these interaction sequences. CircHECTD1 and ROCK2 were upregulated in the rat MIRI model, while miR‐138‐5p was decreased. CircHECTD1 knockdown alleviated H/R‐induced inflammation in H9c2 cells. Direct interaction and regulation of circHECTD1/miR‐138‐5p and miR‐138‐5p/ROCK2 were confirmed by dual‐luciferase assay. CircHECTD1 promoted H/R‐induced inflammation and cell apoptosis by inhibiting miR‐138‐5p. miR‐138‐5p alleviated H/R‐induced inflammation, while ectopic ROCK2 antagonized such effect of miR‐138‐5p. Our research suggested that the circHECTD1‐modulated miR‐138‐5p suppressing is responsible for ROCK2 activation during H/R‐induced inflammatory response, providing a novel insight into MIRI‐associated inflammation.

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Sevoflurane Alleviates Myocardial Ischemia/Reperfusion Injury by Targeting the circ_CDR1as/miR‐671‐5p/HMGA1 Axis

Zhang,

Yang,

Feng

et al. 2024

J Biochem & Molecular Tox

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Sevoflurane (Sev) has a cardioprotective role in myocardial ischemia/reperfusion injury (MI/RI), but its mechanism has not been fully elucidated. This study aimed to investigate whether the circ_CDR1as/miR‐671‐5p/HMGA1 axis mediates the cardioprotective effect of Sev in MI/RI. Cardiomyocytes underwent hypoxia/reoxygenation (H/R) treatment was used to simulate MI/RI in vitro. H/R cardiomyocytes were then pretreated with Sev to explore the protective effect of Sev on H/R cells. The level of CDR1as/miR‐671‐5p/HMGA1 axis were detected by RT‐qPCR. The proliferation and apoptosis of cardiomyocytes were detected by CCK‐8 and flow cytometry. The levels of myocardial injury markers and inflammatory markers were detected by ELISA assay. Finally, the regulatory relationship between CDR1as and miR‐671‐5p/HMGA1 axis was verified by Dual‐luciferase reporting and RNA pull‐down assays. Sev Pretreatment can reduce the level of CDR1as and mitigate H/R‐induced damage to cardiomyocytes. This Pretreatment lowers the levels of myocardial injury markers, oxidative stress markers, and pro‐inflammatory factors in H/R‐affected cardiomyocytes. However, CDR1as overexpression inhibits Sev's protective effect on H/R cardiomyocytes. At the molecular mechanism, we found that CDR1as mediates Sev's protective effect through the CDR1as/miR‐671‐5p/HMGA1 axis. CDR1as increases HMGA1 levels by sponging miR‐671‐5p, while high HMGA1 levels diminish Sev's protective effect. Sev plays a cardioprotective role in MI/RI by inhibiting the circ_CDR1as/miR‐671‐5p/HMGA1 axis.

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Circ_0050908 up-regulates TRAF3 by sponging miR-324-5p to aggravate myocardial ischemia-reperfusion injury

Cited by 12 publications

References 28 publications

ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis

ALKBH5‐mediated m6A demethylation of pri‐miR‐199a‐5p exacerbates myocardial ischemia/reperfusion injury by regulating TRAF3‐mediated pyroptosis

CircHECTD1 promoted MIRI‐associated inflammation via inhibiting miR‐138‐5p and upregulating ROCK2

Sevoflurane Alleviates Myocardial Ischemia/Reperfusion Injury by Targeting the circ_CDR1as/miR‐671‐5p/HMGA1 Axis

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