摘要
Background Experimental evidence indicates that cyclooxygenase-2 (COX-2) plays a critical role in blastocyst implantation; however, little is known of the role of COX-2 in unexplained recurrent spontaneous abortion (URSA). Methods We evaluated the expression level and potential signaling pathway of COX-2 in 30 cases of URSA who were excluded the abnormality of chromosomes, anatomy, endocrine, infectious, autoimmune diseases and in 30 normal pregnancies. Results The mRNA and the protein expression level of COX-2 in the URSA group (-0.238±0.848, 0.368±0.089, respectively) were significantly lower than that in the control group (1.943±3.845, 1.046±0.108, respectively) (both, P 〈0.01). The expression of prostaglandins PGF2a, PGD2, PGE2, and PGI2, in the URSA group ((2326.0±295.6) pg/ml, (2164.0±240.5) pg/ml, (238.7±26.4) pg/ml, (2337.0±263.0) pg/ml, respectively) were significantly lower than that in the control group ((3450.0±421.7) pg/ml, (3174.0±415.6) pg/ml, (323.5±43.8) pg/ml, (3623.0±460.4) pg/ml, respectively) (P 〈0.05). The mRNA expression level of PPARI3 and RXRa (0.859±0.653, -0.172±0.752, respectively) in URSA group was significantly lower than that in the control group (1.554±1.735, 0.777±2.482, respectively) (both P 〈0.05). The mRNA and protein expression levels of vascular endothelial growth factor-A (VEGF-A) in the URSA group (2.010±1.522, 0.35±0.46) was significantly lower than that in the control group (4.569±2.430, 0.750±0.350) (both P 〈0.05). Conclusions COX-2 and the COX-2-derived PGI2 signaling pathway possibly play an important role in successful embryo implantation, and their decreased expression may result in URSA. The decreased expression may influence the expression of VEGF-A which interferes with placental angiogenesis causing failure of embryo implantation, leading to spontaneous abortion.
Background Experimental evidence indicates that cyclooxygenase-2 (COX-2) plays a critical role in blastocyst implantation; however, little is known of the role of COX-2 in unexplained recurrent spontaneous abortion (URSA). Methods We evaluated the expression level and potential signaling pathway of COX-2 in 30 cases of URSA who were excluded the abnormality of chromosomes, anatomy, endocrine, infectious, autoimmune diseases and in 30 normal pregnancies. Results The mRNA and the protein expression level of COX-2 in the URSA group (-0.238±0.848, 0.368±0.089, respectively) were significantly lower than that in the control group (1.943±3.845, 1.046±0.108, respectively) (both, P 〈0.01). The expression of prostaglandins PGF2a, PGD2, PGE2, and PGI2, in the URSA group ((2326.0±295.6) pg/ml, (2164.0±240.5) pg/ml, (238.7±26.4) pg/ml, (2337.0±263.0) pg/ml, respectively) were significantly lower than that in the control group ((3450.0±421.7) pg/ml, (3174.0±415.6) pg/ml, (323.5±43.8) pg/ml, (3623.0±460.4) pg/ml, respectively) (P 〈0.05). The mRNA expression level of PPARI3 and RXRa (0.859±0.653, -0.172±0.752, respectively) in URSA group was significantly lower than that in the control group (1.554±1.735, 0.777±2.482, respectively) (both P 〈0.05). The mRNA and protein expression levels of vascular endothelial growth factor-A (VEGF-A) in the URSA group (2.010±1.522, 0.35±0.46) was significantly lower than that in the control group (4.569±2.430, 0.750±0.350) (both P 〈0.05). Conclusions COX-2 and the COX-2-derived PGI2 signaling pathway possibly play an important role in successful embryo implantation, and their decreased expression may result in URSA. The decreased expression may influence the expression of VEGF-A which interferes with placental angiogenesis causing failure of embryo implantation, leading to spontaneous abortion.