Background. This study was aimed at exploring the biological function and molecular mechanism of ferroptosis of LRP6 modulation in cardiomyocytes of myocardial infarction (MI). Method. We established the ferroptosis model of MI in vivo and in vitro and constructed the modulation network of circRNA-miRNA-LRP6 by bioinformatics analysis; then, we focused on exploring the regulatory relationship of LRP6 and its upstream genes circRNA1615 and miR-152-3p in the RIP experiments and the double luciferase reporter gene assay. Also, we tested the LRP6-mediated autophagy-related ferroptosis in MI. Results. Ferroptosis was found in cardiomyocytes of MI, and ferroptosis inhibitor Ferrostatin-1 (Fer-1) could improve the pathological process of MI. LRP6 was involved in the process of ferroptosis in cardiomyocytes, and LRP6 deletion regulated ferroptosis in cardiomyocytes through autophagy. Screening and identification of the upstream gene circRNA1615 would target LRP6. circRNA1615 inhibited ferroptosis in cardiomyocytes, and circRNA1615 could regulate the expression of LRP6 through sponge adsorption of miR-152-3p, prevent LRP6-mediated autophagy-related ferroptosis in cardiomyocytes, and finally control the pathological process of MI. Conclusions. circRNA1615 inhibits ferroptosis via modulation of autophagy by the miRNA152-3p/LRP6 molecular axis in cardiomyocytes of myocardial infarction.
Background: Coronary artery ectasia (CAE) is an angiographic finding of abnormal coronary dilatation. Inflammation plays a major role in all phases of atherosclerosis. We investigated the relationship between CAE and serum high-sensitivity C-reactive protein (hs-CRP) and interleukin-6 (IL-6) levels to test our hypothesis that patient age is associated with the efficacy of anti-inflammatory therapy for CAE. Methods: We conducted a prospective analysis of 217 patients with CAE treated at the
The role of Hsa_circ_0001445 in oxidation Low Lipoprotein (ox-LDL) induced HUVEC inflammatory damage remains poorly characterized. The present study investigated the performance of the circRNA Hsa_circ_0001445 on ox-LDL-induced HUVEC inflammatory damage. ox-LDL was employed to treat HUVECs and the expression of Hsa_circ_0001445 in cells were detected by qRT-PCR. Then, the overexpression plasmid of circ_0001445 was transfected into HUVECs. The Cell Counting Kit-8 assay was performed to detect cell viability, and the expression of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in treatment cells were measured using ELISAs. Furthermore, the oxidative stress kit was used to detect the levels of malondialdehyde, superoxide dismutase and glutathione peroxidase in treatment cells. Flow cytometry assay was applied to measure cell apoptosis, and the expressions of apoptosis-related protein were measured by western blot. The luciferase reporter assay was applied to confirm the target binding between Hsa_circ_0001445 and micro-RNA-640 (miRNA-640). Next, miRNA-640 mimic was transfected into ox-LDL-induced HUVECs, and then cell proliferation, expression level of inflammatory factors, oxidative stress and apoptosis level in treatment cells were assessed, with the expression of related proteins measured. The results revealed that the expression of Hsa_circ_0001445 was obviously downregulated in ox-LDL-induced HUVECs. Overexpression of Hsa_circ_0001445 promoted cell proliferation, inhibited ox-LDL-induced HUVEC inflammatory response, downregulate the expression of TNF-α, IL-1β and IL-16, overexpression of Hsa_circ_0001445 inhibited cell apoptosis. miRNA-640 was confirmed as a direct target of Hsa_circ_0001445, and miRNA-640 mimic reversed the effects of Hsa_circ_0001445 overexpression on ox-LDL-induced HUVECs. Our findings concluded that Hsa_circ_0001445 inhibits ox-LDL-induced HUVEC inflammation, oxidative stress and apoptosis by regulating miRNA-640.
The function of lncRNA CRNDE and its role in prostate cancer (PC) remains unclear. The aim of this study was to determine the expression level of lncRNA CRNDE in PC tissues and to elucidate its role in PC. The expression levels of lncRNA CRNDE were measured by quantitative reverse transcription polymerase chain reaction. The role of lncRNA CRNDE in PC cells was studied using loss-of-function assays in vitro. Cell proliferation, migration, invasion, and apoptosis were assessed via Cell Counting Kit-8, colony formation, flow cytometry, wound healing, and transwell chamber assays. A luciferase reporter assay was used to characterize the interaction between lncRNA CRNDE and miR-146a-5p. In PC tissues, the expression level of lncRNA CRNDE was upregulated. Moreover, knockdown of lncRNA CRNDE suppressed PC cell proliferation and migration and induced apoptosis in vitro. miR-146a-5p was verified as a direct target of lncRNA CRNDE. Moreover, the inhibition of miR-146a-5p partially counteracted the effects of lncRNA CRNDE on PC cell proliferation, migration, and invasion. In conclusion, lncRNA CRNDE may serve as a cancer promoter in PC by targeting miR-146a-5p. Therefore, lncRNA CRNDE could be a promising target for the clinical treatment of PC.
In Wuhan, China, the first case of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) was reported on December 8, 2019. The patient’s symptoms included fever, coughing and breathing difficulties. According to the sixth China version of 2019 coronavirus disease (COVID-19) diagnostic criteria, some patients with COVID-19 may present atypical symptoms and have negative nucleic acid tests (NATs), possibly leading to misdiagnosis and viral transmission. Our patient was a 29-year-old woman who complained of a three-day history of nasal obstruction, and no fever, coughing or breathing difficulties were noted. Physical examination revealed no obvious signs of pneumonia. On January 16, 2020, the patient flew from Wuhan to Germany for a business trip and returned to Shanghai on January 28, a passenger on her flight was tested positive for SARS-CoV-2 later. Although two consecutive NATs performed at an interval of 24 h were negative, considering her direct contact with a SARS-CoV-2-infected individual, a 64-slice computed tomography (CT) scan showed a few scattered ground-glass nodules in the left lung, suggesting possible viral pneumonia. Given the clinical characteristics, epidemiological records, CT findings and a third positive NAT, our patient was diagnosed with COVID-19. The combination of history of epidemiology, clinical symptom, lung CT scan and routine blood test will improve the clinical diagnosis of asymptomatic COVID-19, but the early diagnosis of COVID-19 can be confirmed only by the repeated NATs.
Background Searching for new molecular targets of ferroptosis is gradually becoming the focus in the field of cardiovascular disease research. This study was aimed to explore the biological function and molecular mechanism of ferroptosis of circRNA modulation in cardiomyocytes of myocardial infarction (MI).Method We explored the regulatory effect and molecular mechanism of LPR6 on myocardial cell ferroptosis by establishing a model of MI in vivo and in vitro, constructed the regulatory network of circRNA-miRNA-LRP6 by the bioinformatics analysis, and focused on the biological function and molecular mechanism of circRNA1615 regulating ferroptosis in MI by the overexpression or knockdown of circRNA1615, the RIP experiments, and double luciferase reporter gene assay.Results Ferrostatin-1(ferroptosis inhibitor) can improve the pathological process of MI; LRP6 was involved in the process of ferroptosis in cardiomyocytes; LRP6 deletion regulates ferroptosis in cardiomyocytes through autophagy; Screening and identification of circRNA1615 targets LRP6; circRNA1615 inhibits ferroptosis in cardiomyocytes; circRNA1615 regulates the expression of LRP6 through sponge adsorption of miR-152-3p, and then prevent LRP6-mediated autophagy-related ferroptosis in cardiomyocytes, finally regulate the pathological process of MI.Conclusions CircRNA1615 inhibits ferroptosis via modulation of autophagy by the miRNA152-3p/LRP6 molecular axis in cardiomyocytes of myocardial infarction.
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