RESUMEN
Coronary atherosclerosis-induced myocardial ischemia leads to cardiomyocyte apoptosis. The regulatory mechanisms for cardiomyocyte apoptosis have not been fully understood. Circular RNAs are non-coding RNAs which play important roles in heart function maintenance and progression of heart diseases by regulating gene transcription and protein translation. Here, we reported a conserved cardiac circular RNA, which is generated from the second exon of LRP6 and named circLRP62-2 . CircLRP62-2 can protect cardiomyocyte from hypoxia-induced apoptosis. The expression of circLRP62-2 in cardiomyocytes was down-regulated under hypoxia, while forced expression of circLRP62-2 inhibited cell apoptosis. Normally, circLRP62-2 was mainly localized in the nucleus. Under hypoxia, circLRP62-2 is associated with heterogeneous nuclear ribonucleoprotein M (hnRNPM) to be translocated into the cytoplasm. It recruited hnRNPM to fibroblast growth factor 9 (FGF9) mRNA to enhance the expression of FGF9 protein, promoting hypoxia-adaption and viability of cardiomyocytes. In summary, this study uncovers a new inhibitor of apoptosis and reveals a novel anti-apoptotic pathway composed of circLRP62-2 , hnRNPM, and FGF9, which may provide therapeutic targets for coronary heart disease and ischemic myocardial injury.
Asunto(s)
MicroARNs , Miocitos Cardíacos , Humanos , Miocitos Cardíacos/metabolismo , ARN Circular/metabolismo , Ribonucleoproteína Heterogénea-Nuclear Grupo M/metabolismo , Factor 9 de Crecimiento de Fibroblastos/metabolismo , Apoptosis/genética , Hipoxia/metabolismo , MicroARNs/genéticaRESUMEN
Mitochondria are the energy production center in cells, which regulate aerobic metabolism, calcium balance, gene expression and cell death. Their homeostasis is crucial for cell viability. Although mitochondria own a nucleus-independent and self-replicating genome, most of the proteins, which fulfill mitochondrial functions and mitochondrial quality control, are encoded by the nuclear genome and are imported into mitochondria. Hence, the regulation of mitochondrial protein expression and translocation is considered essential for mitochondrial homeostasis. By means of high-throughput RNA sequencing and bioinformatic analysis, non-coding RNAs localized in mitochondria have been generally identified. They are either generated from the mitochondrial genome or the nuclear genome. The mitochondrial non-coding RNAs can directly interact with mitochondrial DNAs or transcripts to affect gene expression. They can also bind nuclear genome-encoded mitochondrial proteins to regulate their mitochondrial import, protein level and combination. Generally, mitochondrial non-coding RNAs act as regulators for mitochondrial processes including oxidative phosphorylation and metabolism. In this review, we would like to introduce the latest research progressions regarding mitochondrial non-coding RNAs and summarize their identification, biogenesis, translocation, molecular mechanism and function.
Asunto(s)
ADN Mitocondrial , Mitocondrias , Mitocondrias/genética , Mitocondrias/metabolismo , ADN Mitocondrial/metabolismo , Cromosomas , Núcleo Celular/metabolismo , Homeostasis/genética , Proteínas Mitocondriales/genética , Proteínas Mitocondriales/metabolismoRESUMEN
We report an integrated production of bio-jet fuel, from dehydrogenation of lignin-derived cycloalkanes and deoxygenation of lipid over PtIr/γ-Al2O3 at 400 °C in the absence of hydrogen. The CO generated in situ via lipid decarbonylation is strongly adsorbed by Ir and subsequently undergoes methanation, with the remaining Pt sites catalyzing cycloalkane dehydrogenation.