ABSTRACT
The expression of endothelial nitric oxide synthase traffic inducer (NOSTRIN) in the placenta of the patients with pregnancy induced hypertension (PIH) was detected and its role in the pathogenesis of PIH was studied. The pathological changes in placental vessels were observed by HE staining. NO2-/NO3-, the stable metabolic end products of NO, was measured with nitrate reductase. The eNOS activity in placental tissues was assayed by spectrophotometry. Western blot analysis was applied to detect NOSTRIN expression. The incidence of thickening and fibronoid necrosis of placental vessels was significantly higher in women with PIH than in the normal group (P < 0.01). The levels of placental NO2-/NO3- in PIH patients (27.53 +/- 7.48 micromol/mg) were significantly lower than in normal group (54.27 +/- 9.53 micromol/mg, P < 0.01). The activity of eNOS was significantly decreased in PIH group (12.826 +/- 3.61 U/mg) as compared with that in normal group (21.72 +/- 3.83 U/mg, P < 0.01). Western blot analysis revealed that both groups expressed 58 kD NOSTRIN, but the protein level was significantly higher in women with PIH than in the normal group (P < 0.01). A significant negative correlation existed between the expression of NOSTRIN protein and the activity of eNOS in placental tissue of women with PIH (r = -0.57, P < 0.01). It was concluded that the level of NOSTRIN expression in placenta of women with PIH was increased, which may play an important role in the pathogenesis of PIH.
ABSTRACT
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 0.05); (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.
Subject(s)
Placenta/metabolism , Pre-Eclampsia/metabolism , Pregnancy/metabolism , Pregnancy Proteins/biosynthesis , Pregnancy Proteins/geneticsABSTRACT
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 transcriptionalpolymerase 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 vs4.87±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.
ABSTRACT
The expression of endothelial nitric oxide synthase traffic inducer (NOSTRIN) in the placenta of the patients with pregnancy induced hypertension (PIH) was detected and its role in the pathogenesis of PIH was studied. The pathological changes in placental vessels were observed by HE staining. NO2-/NO3- , the stable metabolic end products of NO, was measured with nitrate reductase. The eNOS activity in placental tissues was assayed by spectrophotometry. Western blot analysis was applied to detect NOSTRIN expression. The incidence of thickening and fibronoid necrosis of placental vessels was significantly higher in women with PIH than in the normal group (P＜0.01). The levels of placental NO2-/NO3- in PIH patients (27.53±7.48 μmol/mg) were significantly lower than in normal group (54.27±9.53 μmol/mg, P＜0.01). The activity of eNOS was significantly decreased in PIH group (12. 826±3.61 U/mg) as compared with that in normal group (21. 72±3.83 U/mg, P＜0.01). Western blot analysis revealed that both groups expressed 58 kD NOSTRIN, but the protein level was significantly higher in women with PIH than in the normal group (P＜0.01). A significant negative correlation existed between the expression of NOSTRIN protein and the activity of eNOS in placental tissue of women with PIH (r=-0. 57, P＜0. 01). It was concluded that the level of NOSTRIN expression in placenta of women with PIH was increased, which may play an important role in the pathogenesis of PIH.
ABSTRACT
Objective To observe the effects of hemin on the expression of hemeoxygenase(HO) on the human umbilical vein endothelial cells.Methods The hemin and zinc protoporphyrin-Ⅸ were added in the cultured endothelial cells to induce and inhibit the expression of HO-1,respectively.The expressions of HO-1 and HO-2 mRNA were detected using reverse transcription polymerase chain(RT-PCR) and the relative amount of CO released into the media was quantitated as carboxyhemoglobin(COHb) by enzyme linked immunosorbent assay(ELISA).The proliferation of endothelial cells was detected by methyl thiazolyl tetrazolium test(MTT).Results The expression of HO protein was mainly detected in the cytoplasm of endothelial cell.The expression of HO-1 mRNA in endothelial cell and the amount of COHb in the media increased significantly with the treatment of hemin.Conclusion The expression of HO-1 and the increase of endogenous CO are the molecular bases of the proliferation of endothelial cells,and the HO/CO system may play an important role in the development of cardiovascular diseases.
ABSTRACT
Objective To investigate the expression and significance of transforming growth factor-beta1(TGF-? 1),transforming growth factor-beta receptor typeⅠ(TGF-? RⅠ) in human ovarian carcinoma. Methods Inmmunohistochemical SP method was used to detect the expression of TGF-? 1 and TGF-? RI in 85 cases of benign and malignant ovarian tumors. Results The positive rate of TGF-? 1 in benign and malignant ovarian tumors was significantly higher than that in the normal ovarian tissues(P