PURPOSE: To investigate the influence of uterine artery embolization (UAE) on endometrial microvessel density (MVD) and angiogenesis. METHODS: Sixty female guinea pigs were divided into two groups, the control group (n = 15) and the UAE treatment group (n = 45). In the UAE group, tris-acryl gelatin microspheres were used to generate embolization. Animals were further divided into three subgroups, A1, A2, and A3 (n = 15 for each subgroup), with uterine specimens collected at 7-15, 16-30, and 31-45 days after UAE, respectively. Immunostaining for factor VIII and CD105 was performed to identify total endometrial MVD (MVDFVIII) and CD105-positive angiogenesis (MVDCD105) at the indicated time points after UAE. RESULTS: Quantitative analysis revealed that MVDFVIII significantly decreased in the A1 (11.40 ± 2.76, p < 0.05) and A2 (15.37 ± 3.06, p < 0.05) groups compared to the control group (19.40 ± 2.50), and was restored to normal in the A3 group (18.77 ± 2.69). UAE caused a temporal up-regulation of MVDCD105-positive angiogenesis in the A1 group (9.33 ± 2.37, p < 0.05) and the A2 group (11.63 ± 1.56, p < 0.05) compared to the control group (7.12 ± 1.67), and the MVDCD105 value returned to normal in the A3 group (8.07 ± 1.97). CONCLUSION: UAE caused a temporal decrease in endometrial MVD that reversed over time as a result of the increase of CD105-positive angiogenesis. Although the UAE-induced reduction of endometrial MVD was reversible, its long-term effect on endometrial receptivity still needs further study.
PURPOSE: To investigate the influence of uterine artery embolization (UAE) on endometrial microvessel density (MVD) and angiogenesis. METHODS: Sixty female guinea pigs were divided into two groups, the control group (n = 15) and the UAE treatment group (n = 45). In the UAE group, tris-acryl gelatin microspheres were used to generate embolization. Animals were further divided into three subgroups, A1, A2, and A3 (n = 15 for each subgroup), with uterine specimens collected at 7-15, 16-30, and 31-45 days after UAE, respectively. Immunostaining for factor VIII and CD105 was performed to identify total endometrial MVD (MVDFVIII) and CD105-positive angiogenesis (MVDCD105) at the indicated time points after UAE. RESULTS: Quantitative analysis revealed that MVDFVIII significantly decreased in the A1 (11.40 ± 2.76, p < 0.05) and A2 (15.37 ± 3.06, p < 0.05) groups compared to the control group (19.40 ± 2.50), and was restored to normal in the A3 group (18.77 ± 2.69). UAE caused a temporal up-regulation of MVDCD105-positive angiogenesis in the A1 group (9.33 ± 2.37, p < 0.05) and the A2 group (11.63 ± 1.56, p < 0.05) compared to the control group (7.12 ± 1.67), and the MVDCD105 value returned to normal in the A3 group (8.07 ± 1.97). CONCLUSION: UAE caused a temporal decrease in endometrial MVD that reversed over time as a result of the increase of CD105-positive angiogenesis. Although the UAE-induced reduction of endometrial MVD was reversible, its long-term effect on endometrial receptivity still needs further study.