To investigate the expressions of placental growth factor (PLGF) in placenta with hypertensive disorders of pregnancy (HDP), 45 women with HDP and 20 normally pregnant women were studied. Among 45 women with HDP, there were 23 cases of severe preeclampsia and one case of eclampsia. The location and level of PLGF proteins was determined by immunohistochemistry and Western blot. The expression of PLGF mRNA in placenta was assessed by reverse transcriptional-polymerase chain reaction (RT-PCR). The results showed that: (1) The distribution of PLGF in placenta with HDP was similar to normal one, which was mainly in the cytoplasm of villous syncytiotrophoblast and villous stroma; (2) The expression of PLGF protein was significantly decreased in placentas with mild and severe preeclampsia compared to the normal ones (0.3±0.4 vs 0.6±0.4, 0.2±0.5 vs 0.6±0.4,P<0.01). There were no differences between the gestational, hypertension placenta and normal one (0.5±0.6 vs 0.6±0.4,P>0.05); (3) The transcription levels of the PLGF mRNA in placentas with preeclampsia were significantly lower than in normal groups (3.33±0.39 vs 4.87±0.60, 1.97±0.29 vs 4.87±0.60,P<0.01), and no differences were found between the gestational hypertension placenta and normal groups. These findings suggest that the abnormal expression of PLGF in placentas is related to the pathogenesis of HDP.

In order to investigate the effects of mouse CTLA4Ig gene-modified dendritic cells (DCs) on the survival of the corneal allografts in rats, the plasmid PG/CTLA4Ig was transfected into DCs of F344 rats mediated by Lipfectamine^TM 2000. The expression of CTLA4Ig was detected by immunofluorescent microscopy. The effects of donor DCs on the proliferation of T cells in Lewis rats (recipients) were tested by by CCK8. Corneal transplantation was performed from F344 rats to Lewis rats. The DCs modified with CTLA4Ig gene were injected into the Lewis rats on the day 0 and 3 after transplantation. The movement of the DCs after modification in vivo was observed by immunofluorescent microscopy, and the survival of corneal allografts was evaluated by Holland criterion. The results showed that the CTLA4Ig-modified DCs could restrain the proliferation of allogenetic T cells. The CTLA4Ig-modified DCs prolonged survival of corneal allografts. (P<0.01). It was suggested that the injection of CTLA4Ig gene-modified DCs could obviously inhabit the allograft rejection and prolong the survival of corneal allografts.

In order to detect the expression of RhoA in placenta from normal pregnancy and preeclampsia and evaluate the role of RhoA in preeclampsia, the expression of RhoA in placenta collected from 40 preeclampsia patients and 20 normotensive controls was determined by immunohistochemistry and RT-PCR. RhoA was found in syncytiotrophoblasts and cytotrophoblasts. The mean density of RhoA protein in placental tissues of mild and severe preeclampsia groups was significantly higher than that in normal pregnancy. The expression level of RhoA mRNA in mild and severe preeclampsia groups was significantly higher than that of normal pregnancy. Increased expression of RhoA in placental tissues might play an important role in the pathogenesis of preeclampsia.