The role of p38α mitogen-activated protein kinase gene in the HELLP syndrome

被引:11
|
作者
Corradetti, Alessandra [1 ]
Saccucci, Franca [2 ]
Emanuelli, Monica [2 ]
Vagnoni, Giorgia [2 ]
Cecati, Monia [2 ]
Sartini, Davide [2 ]
Giannubilo, Stefano R. [1 ]
Tranquilli, Andrea L. [1 ]
机构
[1] Polytech Univ Marche, Dept Clin Sci Obstet & Gynecol, Salesi Hosp, I-60123 Ancona, Italy
[2] Polytech Univ Marche, Dept Biochem Biol & Genet, I-60123 Ancona, Italy
来源
CELL STRESS & CHAPERONES | 2010年 / 15卷 / 01期
关键词
p38 alpha mitogen-activated kinase; HELLP; IUGR; P38 MAP KINASE; ELEVATED LIVER-ENZYMES; CELL-MIGRATION; LOW PLATELETS; PATHWAY; STRESS; DIFFERENTIATION; HEMOLYSIS; GROWTH; PHOSPHORYLATION;
D O I
10.1007/s12192-009-0125-x
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitogen-activated protein kinase (MAPK) p38 alpha was shown to be implicated in the organogenesis of the placenta, and such placental alteration is crucial for the development of hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome. We aimed to analyze for the first time human placental expression of MAPK p38 alpha in pregnancies complicated by HELLP. The placental expression of MAPK p38 alpha was investigated by semiquantitative polymerase chain reaction using cDNA extracted from placental tissue of 15 pregnancies with HELLP syndrome and 15 gestational age-matched controls. Seven patients with HELLP also had intrauterine fetal growth restriction (IUGR). In placenta from pregnancy complicated by HELLP, the expression of MAPK p38 alpha is significantly decreased compared to the group with normal pregnancy (p < 0.001), while no difference was found between the HELLP and HELLP with IUGR subpopulations. Our study shows for the first time that MAPK p38 alpha is expressed in the human placenta. Pregnancies with placental dysfunction and hypertensive complications are characterized by a significantly decreased expression of MAPK p38 alpha. Our observations suggest that p38 MAPK signaling may be essential in placental angiogenesis and functioning.
引用
收藏
页码:95 / 100
页数:6
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