We are analyzing https://link.springer.com/article/10.1007/s10753-024-02116-0.

Title:
ZC3H13-Mediated m6A Modification Ameliorates Acute Myocardial Infarction through Preventing Inflammation, Oxidative Stress and Ferroptosis by Targeting lncRNA93358 | Inflammation
Description:
Background Acute myocardial infarction (AMI) is a life-threatening event that is associated with RNA modification and programmed cell death (PCD). This study attempted to investigate the impacts of zinc finger CCCH domain-containing protein 13 (ZC3H13)-mediated N6-methyladenosine (m6A) on ferroptosis in AMI. Methods The infarcted areas and cardiac function were evaluated, and the expression level of ZC3H13 was measured in AMI rats that were induced by isoproterenol. Meanwhile, oxygen glucose deprivation (OGD) in vitro model was induced to investigate the alterations on inflammation, oxidative stress and ferroptosis. The m6A modification site of lncRNA93358 modified by ZC3H13 was predicted using bioinformatics, and the interaction between ZC3H13 and lncRNA93358 was verified using the dual-luciferase reporter assays. ZC3H13 was overexpressed and lncRNA93358 was silenced to study their regulatory role in cell death, inflammation, oxidative stress and ferroptosis in AMI. Results Significant decreased expression of ZC3H13 was observed in AMI rats, with impaired cardiac function, enhanced inflammation and oxidative stress. ZC3H13 targeted the modification site GGACC of lncRNA93358 and downregulated lncRNA93358. Silencing lncRNA93358 inhibited cell death, reduced the levels of inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β, suppressed oxidative stress-related indicators (lactate dehydrogenase (LDH), reactive oxygen species (ROS), glutathione (GSH) and malondialdehyde (MDA), as well as downregulated ferroptosis-related acyl-CoA synthetase long chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (PTGS2) and glutathione peroxidase 4 (GPX4). The effect of silencing lncRNA93358 was further enhanced by overexpression of ZC3H13. Conclusion This study reveals the ZC3H13-mediated epigenetic RNA modification targeting lncRNA93358 and suggests that ZC3H13 overexpression may be a promising approach for AMI treatment.
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Keywords {🔍}

zch, lncrna, cells, cell, modification, ami, fig, overexpression, group, oxidative, ferroptosis, stress, pubmed, expression, myocardial, silencing, rna, article, ogd, death, rats, control, compared, inflammation, google, scholar, infarction, usa, analysis, decreased, methylation, site, wang, china, stimulation, cardiac, central, zhang, ldh, ros, pcdnanc, versus, assays, viability, content, study, levels, gsh, mda, min,

Topics {✒️}

annexin v-fitc/propidium iodide mettl3-modified lncrna-snhg8 binds alleviate ogd/erastin-induced ferroptosis ogd/erastin + pcdna-nc group hypoxia/reoxygenation-treated myocardial cells rna n6-methyladenosine regulators acute myocardial infarction zc3h13-mediated m6a modification ogd/erastin-treated ac16 cells isoproterenol-induced myocardial infarction ogd-induced m6a modification dual-luciferase reporter assays real-time quantitative pcr 2021 n6-adenosine methylation pcdna-zc3h13 + si-lncrna93358 group hrp-labeled secondary antibodies m6a rna methylation gene symbol abca9-as1 ogd/erastin + pcdna-nc writing—review & editing epigenetic rna modification inflammatory cytokine tnf-α direct rna sequencing mediated n6-methyladenosine oxidative stress-related indicators inflammatory cytokines tnf-α myocardial ischemia/reperfusion injury full access erastin-treated cells compared understanding myocardial infarction promote myocardial infarction gannan medical university time-dependent manners compared infarction size ogd-treated ac16 cells myocardial infarction rats m6a rna modifications modification targets related 100-nt rna fragments myocardial tissue fibers fitc-labeled annexin m6a modification plays m6a modification site ferroptosis-related proteins acsl4 methylated rna immunoprecipitation privacy choices/manage cookies m6a modification involving modification site ggacc search search m6a regulators hnrnpc

Schema {🗺️}

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         description:Acute myocardial infarction (AMI) is a life-threatening event that is associated with RNA modification and programmed cell death (PCD). This study attempted to investigate the impacts of zinc finger CCCH domain-containing protein 13 (ZC3H13)-mediated N6-methyladenosine (m6A) on ferroptosis in AMI. The infarcted areas and cardiac function were evaluated, and the expression level of ZC3H13 was measured in AMI rats that were induced by isoproterenol. Meanwhile, oxygen glucose deprivation (OGD) in vitro model was induced to investigate the alterations on inflammation, oxidative stress and ferroptosis. The m6A modification site of lncRNA93358 modified by ZC3H13 was predicted using bioinformatics, and the interaction between ZC3H13 and lncRNA93358 was verified using the dual-luciferase reporter assays. ZC3H13 was overexpressed and lncRNA93358 was silenced to study their regulatory role in cell death, inflammation, oxidative stress and ferroptosis in AMI. Significant decreased expression of ZC3H13 was observed in AMI rats, with impaired cardiac function, enhanced inflammation and oxidative stress. ZC3H13 targeted the modification site GGACC of lncRNA93358 and downregulated lncRNA93358. Silencing lncRNA93358 inhibited cell death, reduced the levels of inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β, suppressed oxidative stress-related indicators (lactate dehydrogenase (LDH), reactive oxygen species (ROS), glutathione (GSH) and malondialdehyde (MDA), as well as downregulated ferroptosis-related acyl-CoA synthetase long chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (PTGS2) and glutathione peroxidase 4 (GPX4). The effect of silencing lncRNA93358 was further enhanced by overexpression of ZC3H13. This study reveals the ZC3H13-mediated epigenetic RNA modification targeting lncRNA93358 and suggests that ZC3H13 overexpression may be a promising approach for AMI treatment.
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      description:Acute myocardial infarction (AMI) is a life-threatening event that is associated with RNA modification and programmed cell death (PCD). This study attempted to investigate the impacts of zinc finger CCCH domain-containing protein 13 (ZC3H13)-mediated N6-methyladenosine (m6A) on ferroptosis in AMI. The infarcted areas and cardiac function were evaluated, and the expression level of ZC3H13 was measured in AMI rats that were induced by isoproterenol. Meanwhile, oxygen glucose deprivation (OGD) in vitro model was induced to investigate the alterations on inflammation, oxidative stress and ferroptosis. The m6A modification site of lncRNA93358 modified by ZC3H13 was predicted using bioinformatics, and the interaction between ZC3H13 and lncRNA93358 was verified using the dual-luciferase reporter assays. ZC3H13 was overexpressed and lncRNA93358 was silenced to study their regulatory role in cell death, inflammation, oxidative stress and ferroptosis in AMI. Significant decreased expression of ZC3H13 was observed in AMI rats, with impaired cardiac function, enhanced inflammation and oxidative stress. ZC3H13 targeted the modification site GGACC of lncRNA93358 and downregulated lncRNA93358. Silencing lncRNA93358 inhibited cell death, reduced the levels of inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-1β, suppressed oxidative stress-related indicators (lactate dehydrogenase (LDH), reactive oxygen species (ROS), glutathione (GSH) and malondialdehyde (MDA), as well as downregulated ferroptosis-related acyl-CoA synthetase long chain family member 4 (ACSL4), prostaglandin-endoperoxide synthase 2 (PTGS2) and glutathione peroxidase 4 (GPX4). The effect of silencing lncRNA93358 was further enhanced by overexpression of ZC3H13. This study reveals the ZC3H13-mediated epigenetic RNA modification targeting lncRNA93358 and suggests that ZC3H13 overexpression may be a promising approach for AMI treatment.
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         Pathology
         Internal Medicine
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      name:Department of Cardiology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, China
      name:Department of Cardiology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, China
      name:Department of Cardiology, First Affiliated Hospital of Gannan Medical University, Ganzhou City, China
      name:Gannan Medical University, Ganzhou City, China
      name:Department of Pediatric Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial People’s Hospital, Guangzhou City, China

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