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1.
Korean Circulation Journal ; : 364-371, 2015.
Article in English | WPRIM | ID: wpr-225171

ABSTRACT

BACKGROUND AND OBJECTIVES: Apurinic/apyrimidinic endonuclease 1/redox effector factor-1 (APE1/Ref-1) is a multifunctional protein involved in the DNA base excision repair pathway, inflammation, angiogenesis, and survival pathways. We investigated serum APE1/Ref-1 in patients with coronary artery disease (CAD). SUBJECTS AND METHODS: Serum APE1/Ref-1 was measured with a sandwich enzyme-linked immunosorbent assay from 360 patients who received coronary angiograms. They were divided into two groups; a control (n=57) and a CAD group (n=303), the latter included angina (n=128) and myocardial infarction (MI, n=175). RESULTS: The levels of APE1/Ref-1 were higher in the CAD than the control (0.63+/-0.07 vs. 0.12+/-0.07 ng/100 microL, respectively; p<0.01). They were also higher in MI than angina (0.81+/-0.10 vs. 0.38+/-0.11 ng/100 microL, respectively; p<0.01) and different according to the thrombolysis in myocardial infarction (TIMI) flow (0.88+/-0.09 for TIMI flow 0, 1, 2 vs. 0.45+/-0.13 ng/100 microL for TIMI flow 3, p<0.01) in acute coronary syndrome. In correlation analysis, the levels of APE1/Ref-1 were positively correlated with Troponin I (r=0.222; p<0.0001) and N-terminal pro-B type natriuretic peptide (NT-proBNP, r=0.217; p<0.0001) but not high sensitivity to C-reactive protein. Also, they revealed a negative correlation with ejection fraction (EF, r=-0.221; p=0.002). However, there were no significant differences among the three groups, were divided by their levels of APE1/Ref-1, for major adverse cardiovascular events (death, recurrent MI, stroke, revascularization) (8.2 vs. 14.0 vs. 12.5%, p=ns). CONCLUSION: The levels of serum APE1/Ref-1 are elevated in CAD, and are higher in MI than in angina. They are correlated with Troponin I, NT-proBNP, and EF.


Subject(s)
Humans , Acute Coronary Syndrome , Biomarkers , C-Reactive Protein , Coronary Artery Disease , Coronary Vessels , DNA , DNA Repair , Enzyme-Linked Immunosorbent Assay , Inflammation , Myocardial Infarction , Stroke , Troponin I
2.
Chinese Journal of General Surgery ; (12): 826-828, 2010.
Article in Chinese | WPRIM | ID: wpr-386982

ABSTRACT

Objective To study the relationship between graft injury and expression of redox factor-1 in early period after liver transplantation in rats. Methods One hundred and fifty adult male Wistar rats were randomly divided into three groups: liver transplant group, sham surgery group and control group. Animals were sacrificed in each group at different time points: 3,6,9, 12,24 hour after liver transplantation. The changes and significance of the expression of Ref-1 were explored by immunohistochemistry, serology and histopathology. Results Compared with sham surgery group and control group, the expression of Ref-1 protein in transplant group was higher than that in other two groups in early period after liver transplantation ( P < 0. 05 ). In pathology there were lots of inflammation cells infiltration around the portal veins, and cell damage of hepatic tissue, while that in sham surgery and control group was comparatively slight. Serum ALT and AST values reached the peak at 6 ~ 12 h, and decreaced significantly after 12 h ( P < 0. 05 ). Conclusions Graft injury after liver transplantation during early period reaches peak at 6 hour and then decreased. Hepatic ischemic reperfusion injury promotes Ref-1 expression, which in turn compensates for programme cell death induced by the injury.

3.
Chinese Journal of Pathophysiology ; (12)2000.
Article in Chinese | WPRIM | ID: wpr-521703

ABSTRACT

Cerebral ischemia and the aftermath of reperfusion form a hypoxic/hyperoxic sequence of events that can trigger DNA damage in neurons of central nervous system. Neuronal apoptosis will happen without immediate DNA repair. APE/Ref-1 is a multifunctional protein involoved in DNA base excision repair pathway and in redox reguiation of DNA-binding activity of AP-1 family members, which may play an important role in protection of postischemic neuronal damage.

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