Macrophage migration inhibitory factor promoter polymorphisms (-794 CATT5-8): Relationship with soluble MIF levels in coronary atherosclerotic disease subjects.

BACKGROUND: We analyzed the relationship of -794 CATT5-8 MIF polymorphisms with soluble MIF in Coronary Atherosclerotic Disease (CAD) patients. METHODS: A total of 256 patients selected, on which 186 normal-coronary and 70 Coronary artery disease subjects, were recruited in the study (Retrospectively registered). Genotyping of -794 CATT5-8 polymorphisms were performed by PCR and DNA sequencing. Serum MIF levels were measured using an ELISA kit. Patients were classified by coronary angiogram, and CAD based on Gensini's integral degree (angiographic scoring system). RESULTS: The allele frequency and genotype frequency of -794 CATT5-8 did not show any differences in normal-coronary subjects and CAD subjects. In CAD patients, serum MIF levels was lower in CATT (5) subjects than in CATT (7) subjects, while the genotype of -794 CATT5-8 did not show differences in serum MIF levels. In addition, we found a decrease in serum MIF levels in carriers of the (5/5) genotypes the -794 CATT5-8 MIF polymorphisms, although it was not significant. There was no relationship of CAD class and the allele frequency of -794 CATT5-8. CONCLUSIONS: This study found no association between CAD class and -794 CATT5-8 MIF polymorphisms with soluble MIF levels in CAD Subjects. TRIAL REGISTRATION: NCT01750502 (November 2012, Retrospectively registered).

Prognostic value of red cell distribution width in patients undergoing percutaneous coronary intervention: a meta-analysis.

OBJECTIVE: To evaluate the prognostic value of baseline red cell distribution width (RDW) in patients with coronary artery diseases (CADs) undergoing percutaneous coronary intervention (PCI) by conducting a meta-analysis. DESIGN: Systematic review and meta-analysis. DATA SOURCE: PubMed, Embase, Wanfang, CNKI and VIP databases were searched from their inceptions to 19 June 2019. ELIGIBLE CRITERIA: Studies investigating the value of baseline RDW for predicting all-cause mortality, cardiovascular mortality and major adverse cardiac events (MACEs) in patients with CAD undergoing PCI were included. DATA EXTRACTION AND SYNTHESIS: Two authors independently extracted the data and evaluated the methodological quality using the Newcastle-Ottawa Scale. STATA V.12.0 software was applied to produce the forest plots using a random-effect model. RESULTS: Twelve studies (13 articles) involving 17 113 patients were included and analysed. Comparison between the highest and lowest RDW category indicated that the pooled risk ratio (RR) was 1.77 (95% CI 1.32 to 2.37) for all-cause mortality, 1.70 (95% CI 1.25 to 2.32) for cardiovascular mortality and 1.62 (95% CI 1.21 to 2.18) for MACEs. The predictive effect of elevated RDW for all-cause mortality was stronger in the subgroup of patients without anaemia (RR 4.59; 95% CI 3.07 to 6.86) than with anaemia. CONCLUSIONS: This meta-analysis indicated that elevated RDW was associated with higher risk of mortality and adverse cardiac events in patients with CAD undergoing PCI. The value of elevated RDW for predicting all-cause mortality appears to be stronger in patients without anaemia. RDW may be served as a promising prognostic biomarker in patients undergoing PCI.

The effects and mechanism of miR-92a and miR-126 on myocardial apoptosis in mouse ischemia-reperfusion model.

Our objective was to explore the effects of miR-92a and miR-126 on myocardial apoptosis in mouse ischemia-reperfusion model and further investigate the underlying mechanisms. Eighteen Kunming mice were selected and randomly divided into sham operation group and ischemia-reperfusion group with nine mice in each group. Cardiac muscle tissue was stained with Evans blue to confirm myocardial infarction and ischemia. Annexin V/PI double staining was used to detect the apoptotic rate of myocardial cells, and terminal-deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) was used to detect the number of apoptotic cells; Western blot was used to detect expression of Caspase 3 to evaluate the apoptosis of mouse myocardial cells; qRT-PCR was used to detect expression of miR-92a and miR-126 in mouse myocardium, and Western blot was used to detect expression of HSP70 in two groups. Evans blue staining results showed that there was a large area of ischemia in myocardium of ischemia-reperfusion mice with marked infarction, suggesting successful establishment of the model. In sham operation group, myocardial cells were mostly normal cells. Annexin V/PI double staining of flow cytometry result showed that the apoptotic rate was 5.9 % in sham operation group and 37.0 % in ischemia-reperfusion group, respectively. Apoptosis detection results showed that apoptotic index (AI) of myocardial cells in ischemia-reperfusion mice was significantly higher than in sham operation group. In addition, qRT-PCR results showed that miR-92a expression in ischemia-reperfusion group was significantly higher than in sham operation group (F = 32.302, P = 0.000), and miR-126 expression in ischemia-reperfusion group was significantly lower than in sham operation group (F = 41.125, P = 0.000). Moreover, HSP70 detected by Western blot showed that HSP expression in ischemia-reperfusion group was significantly lower than in sham operation group. The change of miR-92a was in accordance with AI of myocardial cells. However, the change of miR-126 is in contrary with AI of myocardial cells, which may be related to the HSP70 expression in myocardial cells.

Presensitized immune condition of host exaggerates prolonged cold ischemia-mediated injury of cardiac graft involving regulatory T cells.

BACKGROUND: The detrimental effect of prolonged cold ischemia time (PCI) on presensitized transplanted graft is conceivable, but the impact of presensitization status of recipient on PCI-mediated graft injury and inflammation is not well defined. METHODS: Allogeneic skin grafts from BALB/c donors were transplanted into C57BL/6 recipients for presensitization. Syngeneic or allogeneic heterotopic heart transplantations with PCI were performed using C57BL/6 or BALB/c donors for these recipients through different treatments. RESULTS: We revealed that PCI could not affect isograft survival but significantly shortened allograft survival in the presensitized recipients. Depletion of regulatory T cells (Tregs) starting 1 day before and after heart transplantation with anti-CD25 monoclonal antibody remarkably induced intragraft Foxp3 gene expression, worsened architecture damage and subepicardial and intramuscle inflammatory cellular infiltration, and caused a dramatic fall of intragraft CD4+/CD8+ ratio, whereas adoptive transfer of exogenous wild-type Tregs or endogenous Tregs promoted by rapamycin had a beneficial effect on preventing the infiltration of T lymphocytes and Gr-1+ neutrophils and reversed intragraft CD4+/CD8+ ratio, preserving cardiac graft architecture. However, their distinct protective mechanisms showed that rapamycin treatment mainly diminished CD4+ T-cell infiltration. Nevertheless, CD4+ still outnumbered CD8+ T cells in the graft, whereas adoptive transfer of Tregs expanded both CD4+ and CD8+ T cells, particularly CD8+ T cells. CONCLUSION: Allogeneic immunoresponses synergistically enhanced PCI effect under presensitized condition. PCI could affect subsequent immunoresponses. Tregs were closely involved in this pathophysiologic process. Our data may pave the way to use Tregs as a novel therapeutic approach to prevent PCI-mediated injury in the presensitized transplant recipients.