Study on p38 mitogen activated protein kinase in vascular endothelial cells dysfunction in preeclampsia
10.3760/cma.j.issn.0529-567x.2011.01.011
- VernacularTitle:p38丝裂原活化蛋白激酶信号分子在子痫前期患者血管内皮细胞损伤中的作用
- Author:
Xin LUO
;
Dandan LIU
;
Hongbo QI
;
Zhenwei YAO
- Publication Type:Journal Article
- Keywords:
Pre-eclampsia;
p38 Mitogen-activated protein kinases;
Endothelium,vascular;
Vascular endothelial growth factor receptor-1;
Receptors,cell surface;
Antigens,CD
- From:
Chinese Journal of Obstetrics and Gynecology
2011;46(1):36-40
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study expression and activation of p38 mitogen activated protein kinase (MAPK) in vascular endothelial cells dysfunction in preeclampsia. Methods From Sept. 2009 to Mar.2010, 54 pregnant women underwent deliveries in the First Affiliated Hospital of Chongqing Medical University were enrolled in this study, including 20 patients in mild preeclampsia group, 16 patients in severe preeclampsia group and 18 women with term cesarean section without perinatal complications as control group. Placental endothelial cells were labeled by CD34 to assay microvessel density (MVD) of each group. Immunohistochemical SP and western blot were used to detect localization and expression of p-p38 MAPK protein, respectively. The levels of sera soluble fms-like tyrosine kinase-1 (sFlt-1)and soluble endoglin(sEng) were measured by ELISA. Results ①The MVD of placenta were 103 ± 3 in control group, 81 ±5 in mild preeclampsia group and 63±4 in severe group, respectively, which showed statistical difference among each group (P＜0.05).②The expression of p38 MAPK protein were 0.84±0.05 in control group,0.90±0.14 in mild group and 0. 86 ±0.18 in severe group, which did not reach remarkable difference among each group (P＞0.05). The expression of p-p38 MAPK protein were 0.13±0.05 in control group,0.59±0.12 in mild group and 1.16±0.18 in severe group, which show statistical difference among each group(P＜0.05).(3) The localization of p-p38 was in trophoblast, endothelial cells and a few (5.2±0.3)and(10.9±0.4)μg/L in control group,(12.5±1.2) and (20.4±5.3)μg/L in mild group and (19.3±3.0) and (29. 5 ±3.7) μg/L in severe group. When drawing paired comparison in those p-p38 MAPK protein levels and the concentrations of serum sFlt-1, sEng in preeclampsia groups (r=0.68,P＜0.05;r=0.87,P＜0.05). Conclusions The remarkable activation of the p38 MAPK in the placenta of patients with preeclampsia induced the increased levels of sFlt-1 and sEng in maternal serum, which confer the injury of vascular endothelial cells that caused the significant decline of MVD in placentas. p38 MAPK signaling might be one of the key pathways in vascular endothelial cell dysfunction in preeclampsia.
