[Expression changes and clinical significance of annexin V in maternal blood and placenta in patients with preeclampsia].

OBJECTIVE

To evaluate the expression of annexin V in maternal blood and placenta, and to explore the relationship between annexin V and preeclampsia (PE).

METHODS

120 women with PE who delivered babies in the Second Hospital of Hebei Medical University from December 2007 to December 2009 were chosen as study groups. They were classified into four groups: early-onset mild group (n = 30), early-onset severe group (n = 30), late-onset mild group (n = 30) and late-onset severe group (n = 30). 30 women without perinatal complications who accepted elective term cesarean section were chosen as control group. Western blot and immunohistochemistry were used to detect the expression and localization of annexin V in placenta and maternal blood. Flow cytometry was employed to detect the apoptosis of cytotrophoblast. AnnexinVmRNA level was determined by reverse transcription (RT)PCR. Prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen (FiB), international normalized ratio (INR) were detected in each group.

RESULTS

(1) The expression of annexin V in placenta and maternal blood were: 0.54 ± 0.12 and 0.62 ± 0.17 in early-onset mild group; 0.47 ± 0.15 and 0.56 ± 0.24 in early-onset severe group; 0.74 ± 0.23 and 1.08 ± 0.32 in late-onset mild group; 0.68 ± 0.28 and 0.72 ± 0.21 in late-onset severe group; 1.73 ± 0.35 and 1.55 ± 0.27 in control group. They were significantly lower in PE groups than in control group (P < 0.05). However, there was no significant difference among PE groups (P > 0.05). (2) The early apoptosis, late apoptosis percentage of trophoblast cells were: 3.21%, 0.86%, in early-onset mild group; 5.32%, 0.72%, in early-onset severe group; 2.43%, 0.63%, in late-onset mild group; 4.28%, 0.48% in late-onset severe group; 1.05%, 0.59%, in control group. Early apoptosis percentage in each group of PE was higher than that in control group (P < 0.05). However, there was no significant difference among PE groups (P > 0.05). (3) The annexin V mRNA levels in placenta were: 25.0 ± 3.0 in early-onset mild group; 24.8 ± 3.0 in early-onset severe group; 25.4 ± 3.9 in late-onset mild group; 25.1 ± 2.7 in late-onset severe group, respectively. All were significantly higher than that in control group (30.6 ± 3.0, P < 0.05), and no significant difference was found among PE groups (P > 0.05). (4) PT, APTT, FiB, INR levels were: (11.3 ± 2.4), (25.6 ± 2.9) s, (4.6 ± 0.9) g/L and 0.9 ± 0.2 in early-onset mild group; (12.1 ± 1.9), (27.2 ± 2.1) s, (5.0 ± 1.0) g/L and 0.9 ± 0.2 in early-onset severe group; (11.7 ± 2.3), (26.5 ± 2.3) s, (5.0 ± 0.7) g/L and 0.8 ± 0.3 in late-onset mild group; (11.4 ± 2.6), (27.3 ± 3.0) s, (4.3 ± 0.8) g/L and 0.8 ± 0.3 in late-onset severe group; (12.4 ± 2.7), (28.0 ± 1.9) s, (5.1 ± 1.2) g/L and 0.9 ± 0.2 in control group. There was no significant difference among PE groups and control group (P > 0.05).

CONCLUSION

The expression changes of annexin V in placenta and maternal blood were observed in patients with PE. This indicated that annexin Vplayed an important role in the pathogenesis and progression of PE by affecting coagulation.