{'fraction_non_alphanumeric': 0.07103825136612021, 'fraction_numerical': 0.07206284153005464, 'mean_word_length': 4.4953095684803, 'pattern_counts': {'":': 0, '<': 1, '<?xml version=': 0, '>': 3, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Expression of Annexin A5 in maternal blood and placenta in pregnancies with preeclampsia


 Background

The placental anticoagulant protein Annexin A5 is highly expressed on the apical surfaces of syncytiotrophoblasts and plays an important role in maintaining blood fluidity in the placental circulation. We investigated the expression of Annexin A5 in maternal blood and placentas from pregnancies complicated by preeclampsia compared with uncomplicated pregnancies.

Materials and Methods

Placental tissue and maternal blood were collected from pregnancies complicated by preeclampsia. They were classified into two groups: early-onset group (n = 10), late-onset group (n = 10) .10 women without perinatal complications who accepted elective term cesarean section were chosen as the control group. Western blot and immunohistochemistry were used to detect the expression and localization of Annexin A5 in the placenta. Annexin A5 mRNA expression was quantified by Real-Time PCR. Annexin A5 and coagulation factor Xa in maternal blood was measured by an enzyme-linked immunosorbent assay. Prothrombin time, activated partial thromboplastin time, Thrombin time, fibrinogen were detected in each groups.

Results

(1) The expression of Annexin A5 in maternal blood were: 5.54±0.29 in early-onset group; 5.10±0.28 in late-onset group; 4.5±0.19 in control group. They were significantly higher in preeclampsia groups than in control group (P = 0.013). However, there was no significant difference among preeclampsia groups (P > 0.05). The mean ±SD coagulation factor Xa expression in the early-onset and late-onset group were 1229.23±45.33 and 1366.96±56.30 versus 1372.95±45.44 in the control group, which has not statistically significant(P=0.072). (2) The protein expression of Annexin A5 in placenta was not statistically significant between the early-onset, late-onset, and control groups (mean ± SD): 0.01 ± 0.02, 0.95±0.03vs.0.99 ± 0.02, p = 0.071.(3) The Annexin A5 mRNA levels in placenta were: 0.79±0.23 in early-onset group; 1.18±0.53 in late-onset group; respectively. All were significantly lower than that in control group (6.19±1.68, P =0.024), and no significant difference was found among preeclampsia groups (P > 0.05). (4) Prothrombin time, activated partial thromboplastin time, Thrombin time, fibrinogen levels were: (11.9 ± 0.23), (33.38± 0.85) s, (16.88 ± 0.45) g/L and 3.85 ± 0.23 in early-onset group; (11.65 ± 0.12), (33.15 ± 0.36) s, (16.13 ± 0.19) g/L and 4.91 ± 0.14 in late-onset group; (12.01 ± 0.09), (32.08 ± 0.41) s, (16.34 ± 0.24) g/L and 4.32 ± 0.20 in control group. The first three were no significant difference among preeclampsia groups and control group (P > 0.05), fibrinogen was statistically significant among all groups (P < 0.05).

Conclusion

These results suggest that Annexin A5 plays an important role in the pathogenesis and progression of preeclampsia by affecting coagulation.