LncRNA LUADT1 sponges miR-195 to prevent cardiac endothelial cell apoptosis in sepsis

Abstract

Background The oncogenic role of the newly identified lncRNA LUADT1 has been revealed in lung adenocarcinoma. It was reported that LUADT1 plays a critical role in multiple human diseases. This study was carried out to investigate the role of LUADT1 in sepsis. Methods Sixty patients with sepsis and sixty healthy volunteers were recruited for this study. Plasma samples were collected from all participants. Human primary coronary artery endothelial cells were also used in this study. The expression of Pim-1, miR-195 and LUADT1 were detected by RT-qPCR. The interaction between miR-195 and LUADT1 was determined by overexpression experiments and luciferase activity assay. Cell apoptosis was detected by flow cytometry. The expression of apoptosis-related protein was detected by Western blotting. Results Bioinformatics analysis revealed the potential interaction between LUADT1 and miR-195, which was confirmed by dual luciferase reporter assay. LUADT1 was downregulated in patients with sepsis. Moreover, LPS treatment downregulated the expression of LUADT1 in primary cardiac endothelial cells. Overexpression of LUADT1 and miR-195 did not affect the expression of each other in primary cardiac endothelial cells. Interestingly, overexpression of LUADT1 was found to upregulate the expression of Pim-1, a target of miR-195. In addition, it was found that overexpression of LUADT1 and Pim-1 reduced the enhancement effects of miR-195 on LPS-induced cardiac endothelial cell apoptosis. Conclusion In summary, LUADT1 may protect cardiac endothelial cells against apoptosis in sepsis by regulating the miR-195/Pim-1 axis.

Release of redox enzymes and micro-RNAs in extracellular vesicles, during infection and inflammation

“…These studies are consistent with the possibility that several miRNA species may be "sponged", i.e., sequestered, by other non-coding RNAs [90] or mRNAs (the so-called "sponges"), potentially including actual miRNA-targets upregulated in sepsis [91]. Alternatively, these could be removed from (or exit) the blood circulation, in sepsis more than in other inflammatory conditions, globally affecting miRNA networks.…”

The Role of Long Non-coding RNAs in Sepsis-Induced Cardiac Dysfunction

“…Overexpression of LUADT1 upregulated the expression of PIM1 , a target of miR-195. These findings indicated that overexpression of either LUADT1 or PIM1 would reduce the damage effects of miR-195 on LPS-induced apoptosis of cardiac endothelial cells ( 83 ). Yu et al ( 84 ) demonstrated that the drug Ulinastatin protected against LPS-induced cell hyperpermeability and apoptosis of cardiac microvascular endothelial cell (CMVECs) via downregulation of lncRNA MALAT1 and EZH2.…”

A bibliometric analysis of cardiomyocyte apoptosis from 2014 to 2023: A review

“…Clinical treatment of SCM mainly includes intervening in septic shock, but a large amount of fluid resuscitation aggravates cardiac load. Studies have shown that autophagy [96,97] and noncoding RNA [98][99][100] are important in the pathogenesis of SCM, and interventions targeting autophagy and noncoding RNA have become a new direction for the treatment or study of SCM.…”