European journal of obstetrics, gynecology, and reproductive biology · 2006
Expression and localization of tumor necrosis factor receptor 1 protein in the chorionic villi in early normal and spontaneous abortion.
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Yu Xuewen, Wang Liqin, Yan Chunfang, Li Xu
Аннотация
BACKGROUND: Increasing tumor necrosis factor alpha (TNFalpha) expression is found to be positively associated with spontaneous abortion. TNFalpha acts through the binding of two types of transmembrane receptors called TNFR1 and TNFR2. Here we compare membrane TNFR1 (mTNFR1) protein expression on chorionic villi in women with spontaneous abortion (SA) and viable pregnancy.
METHODS: In a prospective study, 31 women with SA and 30 with a viable pregnancy were studied. Chorionic villous membrane TNFR1 was detected by confocal laser scanning microscopy and immunohistochemistry.
RESULTS: The mTNFR1 protein is expressed in villous stromal, vessel endothelial, syncytiotrophoblast, and cytotrophoblast cells in early pregnancy. The intensity of mTNFR1 fluorescence (mean+/-S.D.) in villous stromal cells was higher in the abortion groups than in the control group (35.99+/-6.35 versus 32.64+/-5.01; p<0.05). In the abortion groups, villous cytotrophoblast cells were intensely positive for mTNFR1, whereas mTNFR1 staining of vessel endothelial and syncytiotrophoblast cells was significantly lower (p<0.001).
CONCLUSION: Abundant mTNFR1 expression in the cytotrophoblast cells in women with SA may mediate TNFalpha to induce programmed cell death in the mTNFR1-expressing cytotrophoblasts to limit their growth. The over-expressing mTNFR1 in villous stromal cells, mediating TNFalpha effects, may cause pathological changes or tissue damage in chorionic villi locally in nonviable pregnancies.
METHODS: In a prospective study, 31 women with SA and 30 with a viable pregnancy were studied. Chorionic villous membrane TNFR1 was detected by confocal laser scanning microscopy and immunohistochemistry.
RESULTS: The mTNFR1 protein is expressed in villous stromal, vessel endothelial, syncytiotrophoblast, and cytotrophoblast cells in early pregnancy. The intensity of mTNFR1 fluorescence (mean+/-S.D.) in villous stromal cells was higher in the abortion groups than in the control group (35.99+/-6.35 versus 32.64+/-5.01; p<0.05). In the abortion groups, villous cytotrophoblast cells were intensely positive for mTNFR1, whereas mTNFR1 staining of vessel endothelial and syncytiotrophoblast cells was significantly lower (p<0.001).
CONCLUSION: Abundant mTNFR1 expression in the cytotrophoblast cells in women with SA may mediate TNFalpha to induce programmed cell death in the mTNFR1-expressing cytotrophoblasts to limit their growth. The over-expressing mTNFR1 in villous stromal cells, mediating TNFalpha effects, may cause pathological changes or tissue damage in chorionic villi locally in nonviable pregnancies.