Abstract: Abstract: Objective To investigate the relationship between in-stent restenosis (ISR) and phosphorylated c-jun
(reflecting the levels of activator protein-1), CD40L on platelets, tissue factors (TF) and tissue factor pathway inhibitor (TFPI)
in patients with coronary heart disease. Methods A total of 200 patients undergoing percutaneous coronary intervention
(PCI) were recruited in this study. According to the coronary angiography of 1 year after PCI, the patients were divided into
ISR group (n=27) and control group (n=173). The amount of phosphorylated c-jun in leukocyte lysate, TF and TFPI were
measured by enzyme-linked immunosorbent assay (ELISA), while the mean fluorescence intensity about CD40L on platelets
was detected by flow cytometry. Risk factors for ISR were analyzed by multivariate Logistic regression. Results The
absorbance of phosphorylated c-jun, the mean fluorescence intensity about CD40L on platelets, the plasma TF, TFPI and TF/
TFPI were significantly higher in the ISR group than those in the control group (P＜0.01). Correlation analysis showed that
the absorbance of phosphorylated c-jun was positively correlated with the mean fluorescence intensity about CD40L on
platelets, TF and TFPI (rs
=0.766, 0.496 and 0.540, P＜0.05). The mean fluorescence intensity about CD40L on platelets was
positively correlated with TF and TFPI (r=0.652, 0.702, P＜0.05). Multivariate Logistic regression analysis indicated that the
higher mean fluorescence intensity about CD40L on platelets, TF / TFPI were risk factors for ISR (P＜0.05). Conclusion
The high expression of inflammatory markers, phosphorylated c-jun, CD40L and increased expression of TF may promote the
occurrence of ISR after PCI in patients with coronary heart disease.

Key words: coronary restenosis, angioplasty, transluminal, percutaneous coronary, in-stent restenosis, phosphorylated c-jun, CD40L, tissue factors