Objective: To study the mRNA and protein expression of matrix metalloproteinase (MMP) 9, 2, metastasis suppressor gene KiSS-1, tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2 in placenta of preeclampsia patients and their relation to the pathogenesis of preeclampsia.
Methods: Expression of MMP-9, MMP-2, KiSS-1, TIMP-1, TIMP-2 mRNAs and proteins in placenta from 27 cases of preeclampsia, 10 cases of gestational hypertension and 30 cases of normal term pregnant women was detected by semi-quantitative RT-PCR, western blotting, and enzyme activity of MMP-9 and MMP-2 was measured by gelatin zymography.
Results: (1) Expression of MMP-9 and MMP-2 mRNA in placenta of preeclampsia (0.39 +/- 0.05 and 0.71 +/- 0.16) was significantly lower than that in normal term pregnancy (0.78 +/- 0.11 and 1.63 +/- 0.31, P < 0.05). Expression of KiSS-1 and TIMP-1 mRNAs in placenta of preeclampsia (1.97 +/- 0.21 and 1.11 +/- 0.18) was significantly higher than that in normal term pregnancy (0.69 +/- 0.27 and 0.65 +/- 0.19) (P < 0.05.). There was no significant difference in TIMP-2 mRNA level between preeclampsia and normal pregnancy (P > 0.05). (2) Expression of MMP-9 and MMP-2 proteins in preeclampsia (1.07 +/- 0.35 and 0.74 +/- 0.23) was significantly lower than that in normal term pregnancy (2.43 +/- 0.92 and 1.48 +/- 0.78) (P < 0.05). Expression of KiSS-1 and TIMP-1 proteins in placenta of preeclampsia (2.46 +/- 0.39 and 1.51 +/- 0.40) was significantly higher than that in normal pregnancy (0.91 +/- 0.35 and 0.93 +/- 0.56) (P < 0.05). There was no significant difference in TIMP-2 protein level between preeclampsia and normal pregnancy (P > 0.05). (3) Enzyme activity of MMP-9 and MMP-2 in placenta of preeclampsia [(2.67 +/- 0.53) gray level.g(-1).L(-1) and (1.13 +/- 0.28) gray level.g(-1).L(-1))] was significantly lower than that in placenta of normal pregnancy [(8.44 +/- 3.70) gray level.g(-1).L(-1) and (3.87 +/- 1.43) gray level.g(-1).L(-1)] (P < 0.05).
Conclusion: Abnormal expression of MMP-9, MMP-2, KiSS-1 and TIMP-1 can cause insufficiency invasion of trophoblast in preeclampsia and superficial placentation, which may play an important role in the pathogenesis and development of preeclampsia.
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