Premium
Deregulation of c‐Src tyrosine kinase and its downstream targets in pre‐eclamptic placenta
Author(s) -
Irtegun Sevgi,
AkcoraYıldız Dilara,
Pektanc Gulsum,
Karabulut Cagla
Publication year - 2017
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/jog.13350
Subject(s) - proto oncogene tyrosine protein kinase src , phosphorylation , kinase , eclampsia , placenta , p38 mitogen activated protein kinases , medicine , signal transduction , western blot , tyrosine kinase , mapk/erk pathway , microbiology and biotechnology , endocrinology , biology , pregnancy , fetus , biochemistry , gene , genetics
Aim Pre‐eclampsia is a serious pregnancy disorder characterized by the new onset of hypertension and proteinuria in the second trimester of pregnancy. The determination of a key signaling regulatory mechanism involved in placental functions is critical to understanding the pathogenesis of pre‐eclampsia. The aim of this study was to examine the activity of c‐Src and its downstream targets, extracellular signal‐regulated kinase 1/2, p38 and Jun N‐terminal kinase, as well as nuclear factor (NF)‐ĸB in placental tissues collected from women with pre‐eclampsia. Methods Ten pre‐eclamptic (PE) placentas and 10 control placentas were used in this study. The Western blot method was performed to evaluate the c‐Src/ mitogen activated protein kinase/NF‐ĸB signaling pathway in each group. Results c‐Src phosphorylation at Tyr‐416, used as a measure of c‐Src activity, was significantly decreased in PE placentas relative to the control. Reduced c‐Src activity resulted in the suppression of extracellular signal‐regulated kinase 1/2 phosphorylation and a significant reduction in the phosphorylation of p38 and Jun N‐terminal kinase in PE placentas. Moreover, IĸBα phosphorylation was significantly elevated, while NF‐ĸB phosphorylation was suppressed in PE placentas. Conclusions The c‐Src/MAPK/NF‐ĸB signaling pathway may contribute to the pathogenesis of pre‐eclampsia.