Effect on the Production of Soluble Endoglin from Human Choriocarcinoma Cells by Preeclampsia Sera
Citation Aoki Y, Yamamoto T, Fumihisa C, Nakamura A, Asanuma A, Suzuki M. Effect on the production of soluble endoglin from human choriocarcinoma cells by preeclampsia sera. Am J Reprod Immunol 2012; 67: 413–420 Problem The soluble endoglin (sEng) is an antiangiogenic protein that may inhibit TGF‐β...
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Veröffentlicht in: | American journal of reproductive immunology (1989) 2012-05, Vol.67 (5), p.413-420 |
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Zusammenfassung: | Citation Aoki Y, Yamamoto T, Fumihisa C, Nakamura A, Asanuma A, Suzuki M. Effect on the production of soluble endoglin from human choriocarcinoma cells by preeclampsia sera. Am J Reprod Immunol 2012; 67: 413–420
Problem The soluble endoglin (sEng) is an antiangiogenic protein that may inhibit TGF‐β1 signaling and endothelial nitric oxide synthase activation in endothelial cells. The levels of sEng increased in sera obtained from preeclampsia. The factors that increase the sEng in preeclampsia have not been known well. To investigate the factors that may increase sEng in preeclampsia, we examined the effect of preeclampsia sera on the production of sEng from human choriocarcinoma (JEG‐3) cells.
Methods Serum samples were taken from women with normal pregnancy and from those with preeclampsia. JEG‐3 cells were cultured with serum for 24 hrs, and the sEng levels in supernatants and expression of sEng and Hemo oxygenase‐1 (HO‐1) mRNA in cells were measured.
Results The addition of preeclampsia sera into JEG‐3 cells led to increased release of sEng and expression of Eng mRNA. Preeclampsia sera inhibited the expression of HO‐1 mRNA in JEG‐3 cells.
Conclusion The results suggest that preeclampsia sera may increase the protein production of sEng and mRNA expression of Eng from JEG‐3 cells like trophoblast without hypoxia and that in addition to hypoxia, preeclampsia sera may play a role of high level of serum sEng in preeclampsia patients. Decreased HO‐1 activity may relate to increased sEng release. |
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ISSN: | 1046-7408 1600-0897 |
DOI: | 10.1111/j.1600-0897.2011.01086.x |