Mitochondrial DNA Together with miR-142-3p in Plasma Can Predict Unfavorable Outcomes in Patients after Acute Myocardial Infarction

Myocardial infarction is one of the leading causes of death worldwide, despite numerous efforts to find efficient prognostic biomarkers and treatment targets. In the present study, we aimed to assess the potential of six microRNAs known to be involved in cardiovascular diseases, cell-free DNA (cfDNA), and mitochondrial DNA (mtDNA) circulating in plasma to be used as prognostic tools for the occurrence of unfavorable outcomes such as major adverse cardiovascular events (MACE) after acute ST-segment elevation myocardial infarction (STEMI). Fifty STEMI patients were enrolled and monitored for 6 months for the occurrence of MACE. Plasma was collected at three time points: upon admission to hospital (T0), at discharge from hospital (T1), and 6 months post-STEMI (T6). Plasma levels of miR-223-3p, miR-142-3p, miR-155-5p, miR-486-5p, miR-125a-5p, and miR-146a-5p, as well as of cfDNA and mtDNA, were measured by RT-qPCR. Results showed that the levels of all measured miRNAs, as well as of cfDNA and mtDNA, were the most increased at T1, compared to the other two time points. In the plasma of STEMI patients with MACE compared to those without MACE, we determined increased levels of miRNAs, cfDNA, and mtDNA at T1. Hence, we used the levels of all measured parameters at T1 for further statistical analysis. Statistical analysis demonstrated that all six miRNAs and cfDNA plus mtDNA levels, respectively, were associated with MACE. The minimal statistical model that could predict MACE in STEMI patients was the combination of mtDNA and miR-142-3p levels, as evidenced by ROC analysis (AUC = 0.97, p < 0.001). In conclusion, the increased plasma levels of mtDNA, along with miR-142-3p, could be used to predict unfavorable outcomes in STEMI patients

Regulation of proline accumulation and its molecular and physiological functions in stress defence

The accumulation of proline is a conserved response of plants to abiotic stress conditions. Moreover, the activation of proline metabolism takes place during the plant response to some pathogens. Although these responses are well documented, the molecular and physiological functions of proline accumulation under stress are still a matter of debate. The biochemical pathways that lead to proline accumulation and its functions in regulating development are described in the cognate chapter “Proline Metabolism and its Functions in Development”. In this chapter, we will describe the potential roles assigned to proline accumulation, dissecting the data coming from in vitro/in silico and in vivo approaches, and those coming from bacterial or unicellular eukaryotes and plants. With this, we aim to present a clear view of the evidence related to the molecular and physiological functions of proline accumulation under stress conditions in plants. In recent years, the understanding of the regulation of proline accumulation at transcriptional level under stress conditions in plants has been increased considerably, yet little is known about the possible occurrence of post-translational regulatory mechanisms. We will integrate this knowledge with the potential roles of proline accumulation to see whether it contributes to comprehending which roles might be physiologically more relevant