Relationship between vascular endothelial growth factor and microvessel density in placenta and placenta increta

Objective To investigate the relationship between the expression level of vascular endothelial growth factor (VEGF) and microvessel density (MVD) in placenta tissue and placenta increta. Methods Thirty singleton pregnant women who received antenatal care and underwent cesarean section in Fujian Maternity and Child Health Hospital between November 2013 and August 2014, were enrolled in this study. They were divided into placenta previa group, placenta increta group and control group, with ten patients in each group. Placenta tissue was collected from each patient. Expressions of VEGF and its mRNA were detected by immunohistochemistry, Western blot, and real-time polymerase chain reaction. MVD in placenta tissue was measured by immunohistochemistry. Rank sum test, t test, Kruskal Wallis test, one-way ANOVA and Spearman correlation test were used for statistical analysis. Results (1) Gestational age at admission and delivery in placenta previa and placenta increta groups was lower than in control group (all P<0.05). Compared with control group, the placenta previa and placenta increta groups had more blood loss, and longer operating duration and hospital stay (all P<0.05). (2) The expression levels of VEGF and its mRNA in placenta increta and placenta previa groups were higher than in control group (VEGF: 0.691±0.032, 0.695±0.027 and 0.518±0.025, respectively, F=373.401; VEGF mRNA: 1.667±0.661, 1.832±0.678 and 0.767±0.269, respectively, F=27.399; both P<0.05). But there was no significant difference between placenta previa and increta groups. (3) There was no significant difference of VEGF expression in increta location, border site and normal site in placenta increta group, but its mRNA was decreasing (2.519±0.116, 1.482±0.232 and 1.000±0.000, respectively, F=240.827, P<0.05). (4) Expression level of VEGF at the attachment of umbilical cord, upper and lower margin of placenta in placenta previa group was higher than in control group (0.702±0.026 vs 0.528±0.020, t=12.302; 0.698±0.026 vs 0.519±0.035, t=12.715; and 0.685±0.029 vs 0.509±0.010, respectively, t=17.891; all P<0.05). Expression of VEGF mRNA in placenta previa group was higher than in control group (2.080±0.539 vs 1.024±0.272, t=8.093; 1.587±0.757 vs 0.546±0.083, t=2.401; 1.828±0.704 vs 0.731±0.157, t=4.259; all P<0.05). (5) MVD in placenta increta group and placenta previa group was higher than in control group (171.2±14.7, 155.7±14.6 vs 147.8±12.3, respectively, F=7.277, P<0.05). (6) Expression level of VEGF in placenta increta group and control group was positively associated with MVD (r=0.825, P<0.05). Conclusions There may be some common mechanisms in the occurrence of placenta previa and placenta increta. Overexpression of VEGF in placenta and abnormal formation of villous vessels may be important factors in the pathogenesis of placenta increta. Key words: Placenta accreta; Placenta previa; Vascular endothelial growth factor A; Placenta; Microvessels