[Alteration and potential role of soluble fms-like tyrosine kinase receptor 1 in preeclampsia].

OBJECTIVE: To investigate the alteration of serum soluble fms-like tyrosine kinase receptor 1 (sFlt-1) and the possible source in preeclampsia, and the relationship between sFlt-1 and the pathogenesis of preeclampsia.

METHODS: (1) Semi-quantitative RT-PCR was carried out to detect the level of sFlt-1 mRNA in placental tissue of 10 preeclampsia (preeclampsia group) and 10 normotensive pregnancies (normotensive pregnancy group). (2) Enzyme linked immunosorbent assay (ELISA) was used to detect the serum level of sFlt-1 in peripheral venous blood in preeclampsia group 1 (n = 35) and normotensive pregnancies group 1 (n = 35); the serum level of sFlt-1 of uterine vein blood in preeclampsia group 2 (n = 20) and normotensive pregnancies group 2 (n = 20); and the volume of peripheral venous blood sFlt-1 in 10 early (early pregnancy group) and 10 middle pregnancies (middle pregnancy group).

RESULTS: (1) sFlt-1 mRNA of placental tissue was significantly higher in preeclampsia group (0.95 +/- 0.04) than that in normal pregnancy group (0.64 +/- 0.15). (2) The serum level of sFlt-1 of peripheral vein in preeclampsia group 1 (5640 +/- 3191) ng/L was higher than that in normal pregnancy group 1 (2194 +/- 635) ng/L. (3) The serum sFlt-1 of uterine vein in preeclampsia group 2 (7673 +/- 2296) ng/L was higher than that in normotensive pregnancy group 2 (3057 +/- 785) ng/L, indicating that the volume of sFlt-1 of uterine vein blood was significantly higher than that of peripheral venous blood (P < 0.01). (4) The serum levels of sFlt-1 in early and middle pregnancy groups were (32 +/- 20) ng/L and (994 +/- 302) ng/L, respectively, showing that the level of sFlt-1 in peripheral venous blood increasingly elevated with the development of pregnancy.

CONCLUSIONS: (1) The placenta may be the major source of elevated sFlt-1. (2) The serum level of sFlt-1 is related with the development of pregnancy. The alteration of sFlt-1 may contribute to the pathogenesis of preeclampsia.