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【medical-news】uNK细胞与反复流产的关系
BACKGROUND: Increased numbers of phenotypically unusual CD56bright CD16– uterine natural killer (uNK) cells have been associated with recurrent reproductive failure. uNK cells produce angiogenic growth factors and are potential regulators of decidual angiogenesis in early pregnancy. The final common mechanism for early pregnancy loss is thought to be early onset of the maternal circulation and excessive placental oxidative stress. We tested the hypothesis that increased uNK cells in preimplantation endometrium are associated with altered angiogenesis.
METHODS: Women with recurrent reproductive failure (n = 122) were investigated with uterine artery Doppler and endometrial biopsy. Immunohistochemistry was used to identify uNK, endothelial and vascular smooth muscle cells and image analysis was used to assess location, density and differentiation.
RESULTS: uNK cell density was positively correlated with the formation of blood (P = 0.005, r = 0.5) and lymphatic vessels (P = 0.0001, r = 0.6), spiral arteriole smooth muscle differentiation (P = 0.01, r = 0.5) and endometrial oedema (P = 0.004). The functional effect of this was a reduced uterine artery resistance to blood flow.
CONCLUSIONS: These data suggest that uNK cells may regulate angiogenesis in non-pregnant endometrium. The mechanisms of reproductive failure associated with increased uNK cell density appear to be increased angiogenesis and peri-implantation blood flow, which may lead to early maternal circulation and hence pregnancy failure due to excessive oxidative stress.
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BACKGROUND: Increased numbers of phenotypically unusual CD56bright CD16– uterine natural killer (uNK) cells have been associated with recurrent reproductive failure. uNK cells produce angiogenic growth factors and are potential regulators of decidual angiogenesis in early pregnancy. The final common mechanism for early pregnancy loss is thought to be early onset of the maternal circulation and excessive placental oxidative stress. We tested the hypothesis that increased uNK cells in preimplantation endometrium are associated with altered angiogenesis.
背景：表型特殊的CD56+CD16-的子宫自然杀伤细胞的增多与复发性流产相关。uNK细胞产生促血管生长因子，并且在孕早期是蜕膜血管生成的潜在调节者。一般认为早期流产的最终机制是母体血循的早期发生和过多的胎盘氧化应激。我们检验了植入前子宫内膜uNK细胞增多与血管生成的改变相关的假说。
METHODS: Women with recurrent reproductive failure (n = 122) were investigated with uterine artery Doppler and endometrial biopsy. Immunohistochemistry was used to identify uNK, endothelial and vascular smooth muscle cells and image analysis was used to assess location, density and differentiation.
方法：检测了122名习惯性流产女性的子宫动脉超声多普勒监测和内膜活检。使用免疫组化来检测uNK细胞，内膜和血管平滑肌细胞，使用图像分析来确定位置、密度和分化程度。
RESULTS: uNK cell density was positively correlated with the formation of blood (P = 0.005, r = 0.5) and lymphatic vessels (P = 0.0001, r = 0.6), spiral arteriole smooth muscle differentiation (P = 0.01, r = 0.5) and endometrial oedema (P = 0.004). The functional effect of this was a reduced uterine artery resistance to blood flow.
结果：uNK密度和血管(P = 0.005, r = 0.5)和淋巴管(P = 0.0001, r = 0.6)生成，螺旋动脉平滑肌分化(P = 0.01, r = 0.5)，内膜水肿(P = 0.004)成正相关。这种功能作用降低了子宫动脉对血流的抵抗。
CONCLUSIONS: These data suggest that uNK cells may regulate angiogenesis in non-pregnant endometrium. The mechanisms of reproductive failure associated with increased uNK cell density appear to be increased angiogenesis and peri-implantation blood flow, which may lead to early maternal circulation and hence pregnancy failure due to excessive oxidative stress.
结论：这些数据显示uNK细胞可能调节非妊娠的子宫内膜的血管生成。流产机制与uNK密度增加相关，是由于血管生成和植入前血流的增加。后者导致了早期母体血循，以及因此过多的氧化应激导致妊娠丢失。
编译：
背景：表型特殊的CD56+CD16-的子宫自然杀伤细胞的增多与复发性流产相关。uNK细胞产生促血管生长因子，并且在孕早期是蜕膜血管生成的潜在调节者。一般认为早期流产的最终机制是母体血循的早期发生和过多的胎盘氧化应激。我们检验了植入前子宫内膜uNK细胞增多与血管生成的改变相关的假说。
方法：检测了122名习惯性流产女性的子宫动脉超声多普勒监测和内膜活检。使用免疫组化来检测uNK细胞，内膜和血管平滑肌细胞，使用图像分析来确定位置、密度和分化程度。
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作者:admin@医学,生命科学 2011-04-07 18:32
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