MOESM7 of Peripheral T cell receptor beta immune repertoire is promptly reconstituted after acute myocardial infarction

Additional file 7: Table S6. The distribution of AA usage in CDR3

MOESM4 of Peripheral T cell receptor beta immune repertoire is promptly reconstituted after acute myocardial infarction

Additional file 4: Table S3. The distribution of V-J combinations in each sample

MOESM3 of Peripheral T cell receptor beta immune repertoire is promptly reconstituted after acute myocardial infarction

Additional file 3: Table S2. The distribution of V and J gene segments in each sample

MOESM2 of Peripheral T cell receptor beta immune repertoire is promptly reconstituted after acute myocardial infarction

Additional file 2: Table S1. The analysis of TCRβ immune repertoire sequencing data

MOESM1 of Peripheral T cell receptor beta immune repertoire is promptly reconstituted after acute myocardial infarction

Additional file 1: Fig. S1. Two-round nested amplicon arm-PCR for TCRβ immune repertoire. n = 5 per group. Fig. S2. The clonotypes analysis of TCRβ base sequence. a Quantification (plot grays) and frequencies (plot colors) of base sequence clonotypes. Light grays indicate the overlapping clonotypes, while dark grays indicate the total clonotypes per sample. b Comparison of total clonotypes of TCRβ base sequence. c The percentage of overlapping base sequence between healthy controls and AMI patients. Fig. S3. The distribution of CDR3 AA length between healthy controls and AMI patients. n = 5 per group

MOESM5 of Peripheral T cell receptor beta immune repertoire is promptly reconstituted after acute myocardial infarction

Additional file 5: Table S4. The distribution of V-D-J combinations in each sample

MOESM6 of Peripheral T cell receptor beta immune repertoire is promptly reconstituted after acute myocardial infarction

Additional file 6: Table S5. The distribution of CDR3 AA clonotypes in each sample

Table_9_Circular RNA-Expression Profiling Reveals a Potential Role of Hsa_circ_0097435 in Heart Failure via Sponging Multiple MicroRNAs.XLSX

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.</p

Table_7_Circular RNA-Expression Profiling Reveals a Potential Role of Hsa_circ_0097435 in Heart Failure via Sponging Multiple MicroRNAs.XLS

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.</p

Table_8_Circular RNA-Expression Profiling Reveals a Potential Role of Hsa_circ_0097435 in Heart Failure via Sponging Multiple MicroRNAs.XLS

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.</p