Fig 1: (A) Cardiac Troponin I (cTnI) levels in plasma collected from pigs treated with 0.078 mg/kg ApTOLL or Placebo at 8 and 24 h after ischemia/reperfusion (IR) (N = 10/group, mean ± SD * p < 0.002 ApTOLL). (B) Left ventricle ejection fraction levels detected by cardiac ultrasound at the times indicated. Representative M-Mode images from Placebo and ApTOLL treated animals, in which end diastolic and systolic thickness of the interventricular septum thickness (IVS) and left-ventricle posterior wall thickness (LVPW) are represented (N = 10/group (d0), N = 9 ApTOLL/8 Placebo (d3, and d7). Mean ± SD * p < 0.001 ApTOLL vs. Placebo).
Fig 2: Pearson correlation coefficient analysis of the relationship between the expression levels of miR-146b and miR-155, and concentrations of the parameters related with myocarditis in Treg cells. (A) The relationship between the expression levels of miR-146b and concentration of CK-MB. (B) The relationship between the expression levels of miR-146b and concentration of cTnI. (C) The relationship between the expression levels of miR-146b and concentration of GrB. (D) The relationship between the expression levels of miR-146b and concentration of sFasL. (E) The relationship between the expression levels of miR-146b and concentration of caspase-3. (F) The relationship between the expression levels of miR-155 and concentration of CK-MB. (G) The relationship between the expression levels of miR-155 and concentration of cTnI. (H) The relationship between the expression levels of miR-155 and concentration of GrB. (I) The relationship between the expression levels of miR-155 and concentration of sFasL. (J) The relationship between the expression levels of miR-155 and concentration of caspase-3. There is a strong positive relation between two variables if rho falls within from 0.5 to 1. The levels of CK-MB, cTnI, GrB, and sFasL were positively associated with the levels of miR-146b and miR-155.
Fig 3: Expression levels of miR-133a and endothelial injury markers (vWF, H-FABP and cTnI) in a rat model of acute myocardial infarction. (A) Quantification of the expression levels of miR-133a in model rats, as determined by RT-qPCR. Expression levels of (B) vWF, (C) H-FABP and (D) cTnI in model rats, as determined by ELISA. Data are presented as the mean ± standard deviation. *P<0.05 vs. the Con group; #P<0.05 vs. the Model group; &P<0.05 vs. the Mimic group. Con: Control group, rats that underwent the sham operation were injected with a vector; Model: Model group, rats in the AMI model group were injected with NC; mimic, miR-133a mimic group, rats in the AMI model group were injected with a miR-133a mimic; inhibitor, miR-133a inhibitor group, rats in the AMI model group were injected with a miR-133a inhibitor; cTnI, cardiac troponin I; H-FABP, heart-type fatty acid-binding protein; miR-133a, microRNA-133a; vWF, Von Willebrand factor.
Fig 4: Expression levels of miR-133a and endothelial injury markers (vWF, H-FABP and cTnI) in patients with or without AMI. The expression levels of miR-133a, and vWF, H-FABP and cTnI, were detected in patients using reverse transcription-quantitative polymerase chain reaction and ELISA, respectively. AMI patients, patients with AMI following radical surgery for gastric cancer; Control patients, patients without AMI following radical surgery for gastric cancer. Data are presented as the mean ± standard deviation. *P<0.05 vs. the Control patients. AMI, acute myocardial infarction; cTnI, cardiac troponin I; H-FABP, heart-type fatty acid-binding protein; miR-133a, microRNA-133a; vWF, Von Willebrand factor.
Supplier Page from Abcam for Human Cardiac Troponin I ELISA Kit