This study aimed to evaluate the potential of long noncoding RNAs (lncRNAs) as biomarkers for coronary artery disease (CAD). We measured the levels of three atherosclerosis‐ or cardiac‐related lncRNAs in peripheral blood monocyte cells (PBMCs) from 20 CAD patients and 20 non‐CAD control participants using real‐time reverse transcription–polymerase chain reaction (real‐time RT–PCR) methods. We found that the levels of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1), hypoxia‐inducible factor 1 alpha‐antisense RNA 2 (HIF1A‐AS2) and apolipoprotein A‐1 antisense RNA (APOA1‐AS) were significantly increased in CAD patients (KCNQ1OT1 increased by 2.38‐fold, P = 0.00042; HIF1A‐AS2 increased by 2.00‐fold, P = 0.0001; APOA1‐AS increased by 4.52‐fold, P = 0.000048). The area under the ROC curve was 0.865 for KCNQ1OT1, 0.852 for HIF1A‐AS2, and 0.967 for APOA1‐AS. Furthermore, the combination of lncRNAs resulted in a much higher AUC value of 0.990 for the prediction of CAD. Spearman's correlation analysis showed that APOA1‐AS was positively correlated with NT‐proBNP, CKMB, MYO and HsTnT, whereas HIF1A‐AS2 was correlated with NT‐proBNP and HsTnT. Hence, the elevation of KCNQ1OT1, HIF1A‐AS2 and APOA1‐AS predicts CAD and these molecules may be considered as novel biomarkers of CAD.

Circular RNAs represent a new type of non-coding RNA molecules that influence the occurrence and development of various human diseases by sponging microRNAs, although their roles in heart failure have not been clarified. In this study, peripheral blood samples from 5 patients with heart failure and 4 healthy volunteers were analyzed by next-generation sequencing (NGS) to screen for differentially expressed Circular RNAs. Fifty-six differentially expressed Circular RNAs were identified, of which 29 were up-regulated and 27 were down-regulated. Dysregulated expression of 6 Circular RNAs was verified by quantitative polymerase chain reaction (PCR) analysis, and hsa_circ_0097435 expression was confirmed to be significantly up-regulated in 40 patients with heart failure. Further study with extracted exosomes showed that hsa_circ_0097435 expression was significantly higher in patients with heart failure. In cardiomyocytes, hsa_circ_0097435 was up-regulated after doxorubicin treatment, promoting cardiomyocyte apoptosis. Hsa_circ_0097435 overexpression promoted cardiomyocyte apoptosis, and silencing hsa_circ_0097435 inhibited apoptosis. Moreover, RNA-pulldown experiments and AGO2-immunoprecipitation experiments revealed that hsa_circ_0097435 potentially served a role in heart failure by sponging multiple microRNAs. Collectively, these results suggest that hsa_circ_0097435 can be used as a biological blood marker and revealed a new pathway involved in regulating myocardial cell injury. Our findings may provide a rational basis for developing new treatments for heart failure.

Circulating miR-22-5p and miR-122-5p could be considered promising novel diagnostic biomarkers for AMI.

The use of circulating microRNAs as biomarkers opens up new opportunities for the diagnosis of cardiovascular diseases because of their specific expression profiles. The aim of the present study was to identify circulating microRNAs in human plasma as potential biomarkers of heart failure and related diseases. We used real-time quantitative PCR to screen mi-croRNA in plasma samples from 62 normal controls and 62 heart failure samples. We found that circulating miR-21-5p, miR-30a-3p, miR-30a-5p, miR-155-5p, miR-216a and miR-217 expressed differently between healthy controls and heart failure patients. Plasma levels of miR-21-5p, miR-30a-3p, miR-30a-5p, miR-155-5p, miR-216a and miR-217 were unaffected by hemolysis. Correlation analysis showed any two of these miRNAs possess a strong correlation, indicating a possibility of combined analysis. MiR-21-5p, miR-30a-3p, miR-30a-5p, miR-155-5p, miR-216a and miR-217 could be combined in two or three or more combinations. The results suggest that miR-21-5p, miR-30a-3p, miR-30a-5p, miR-155-5p, miR-216a and miR-217 may be a new diagnostic biomarker for heart failure and related diseases.

Alginate oligosaccharide (AOS) has recently demonstrated the ability to protect against acute doxorubicin cardiotoxicity and neurodegenerative disorders by inhibiting oxidative stress and endoplasmic reticulum (ER) stress-mediated apoptosis, which are both involved in myocardial ischemia/reperfusion (I/R) injury. In the present study, we investigated whether pretreatment with AOS protects against myocardial I/R injury in mice and explored potential cardioprotective mechanisms. AOS pretreatment significantly decreased the infarct size, reduced the cardiac troponin-I concentration, and ameliorated the cardiac dysfunction. Accompanied with the reduced cardiac injury, AOS pretreatment clearly decreased I/R-induced myocardial apoptosis. With regard to mechanism, AOS pretreatment markedly attenuated nitrative/oxidative stress, as evidenced by decreases in 3-nitrotyrosine content and superoxide generation, and downregulated inducible nitric oxide synthase, NADPH oxidase2, and 4-hydroxynonenal. Moreover, AOS pretreatment decreased myocardial apoptosis by inhibiting the ER stress-mediated apoptosis pathway, which is reflected by the downregulation of C/EBP homologous protein, glucose-regulated protein 78, caspase-12, and Bcl-2-associated X protein, and by the upregulation of the anti-apoptotic protein B-cell lymphoma-2. Collectively, these findings demonstrate that AOS renders the heart resistant to I/R injury, at least in part, by inhibiting nitrative/oxidative stress and ER stress-mediated apoptosis.

BackgroundAcute myocardial infarction (AMI) is characterized by an inflammatory process in which T cell plays a key role. However, the profile of immune microenvironment in AMI is still uncertain. High-throughput sequencing of T cell receptor (TCR) provides deep insight into monitoring the immune microenvironment.Methods30 patients with AMI were enrolled and 30 healthy individuals were recruited as controls. Flow cytometer were used to analyze the distribution of αβ T cells and their CD69 expression from peripheral leukomonocytes. TCRβ repertoire library was amplified by two-round multiplex PCR and detected by next-generation sequencing (NGS).ResultsThe percentage of αβ T cells in AMI patients were significantly restricted than those in healthy controls, while the highly activated αβ T cells along with distinguishing usage of variable (V), diversity (D) and joining (J) gene segments were also found in AMI patients. In addition, AMI induced a significantly restricted CDR3 amino acid (AA) diversity and remarkably reconstituted TCR immune repertoires. Finally, we identified several AMI-associated tendency of CDR3 AAs expression after AMI.ConclusionsOur work suggests that the aberrant αβ T cells distribution and activation may associated with the pathogenesis of AMI and demonstrates a reconstitution of TCRβ immune repertoire after AMI.Electronic supplementary materialThe online version of this article (10.1186/s12967-019-1788-4) contains supplementary material, which is available to authorized users.

In this study, the complete mitochondrial genome of human lung fluke, Paragonimus heterotremus, was recovered through Illumina sequencing data. This complete mitochondrial genome of P. heterotremus is 13,927 bp in length and has a base composition of A (16.6%), T (41.8%), C (13.%), G (28.4%), demonstrating an obvious bias of high AT content (58.4%). The mitochondrial genome contains a typically conserved structure, encoding 12 protein-coding genes (PCGs), 22 transfer RNA genes (tRNA), 2 ribosomal RNA genes (12S rRNA and 16S rRNA) and a control region (D-loop region). All PCGs were located on the H-strand. ND4 gene and ND4L gene were overlapped by 39 bp. The nucleotide sequence of 12 PCGs of P. heterotremus and other 10 parasite species were used for phylogenetic analysis. The result indicated P. heterotremus a relative close relationship with species Paragonimus westermani (AF219379.2).

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