MicroRNA-155 inhibits migration of trophoblast cells and contributes to the pathogenesis of severe preeclampsia by regulating endothelial nitric oxide synthase.
نویسندگان
چکیده
The aim of the present study was to characterize the role of microRNA (miR)-155 in the pathogenesis of severe preeclampsia (PE). A total of 19 severe preeclampsic and 22 normal placentas were collected to measure miR-155 and endothelial nitric oxide synthase (eNOS) expression using quantitative (q)PCR and western blot analysis. The results demonstrated a significant increase in the levels of miR-155 and decreased eNOS expression in the severe preeclampsic placentas, as compared with the normal controls. In order to examine the function of miR-155 in the human placenta, the HTR8/Svneo cell line was transiently transfected with an miR-155 mimic or its inhibitor, anti-miR-155. It was confirmed that miR-155 may suppress the expression of eNOS in HTR-8/SVneo cells. Furthermore, a transwell insert invasion assay demonstrated that miR-155 inhibited cell invasion in trophoblast cells, and the effect was rescued by over expression of eNOS. The present study revealed that miR-155 has a negative regulatory role in the migratory behavior of HTR-8/SVneo cells via modulating eNOS.
منابع مشابه
EXPRESSION OF INDUCIBLE NITRIC OXIDE SYNTHASE GENE (iNOS) STIMULATED BY HYDROGEN PEROXIDE IN HUMAN ENDOTHELIAL CELLS
Inducible nitric oxide synthase (iNOS) gene expresses a calcium calmudolin-independent enzyme which can catalyse NO production from L-arginine. The induction of iNOS activity has been demonstrated in a wide variety of cell types under stimulation with cytokines and lipopoly saccharide (LPS). Previous studies indicated that all nitric oxide synthases (NOS) activated in human umbilical vein endot...
متن کاملSpironolactone Inhibits NADPH Oxidase-Mediated Oxidative Stress and Dysregulation of the Endothelial NO Synthase in Human Endothelial Cells
Accumulating evidence indicates that aldosterone plays a critical role in the mediation of oxidative stress and vascular damage. NADPH oxidase has been recognized as a major source of oxidative stress in vasculature. However, the relation between NADPH oxidase in aldosterone-mediated oxidative stress in endothelial cells remains to be ascertained. The present study aimed to investigate the rel...
متن کاملNitric Oxide Functions; an Emphasis on its Diversity in Infectious Diseases
Nitric oxide is a short-lived mediator, which can be induced in a variety of cell types and produces many physiologic and metabolic changes in target cells. It is important in many biological functions and generated from L-arginine by the enzyme nitric oxide synthase. Nitric oxide conveys a variety of messages between cells, including signals for vasorelaxation, neurotransmission and cytotoxici...
متن کاملSpironolactone Inhibits NADPH Oxidase-Mediated Oxidative Stress and Dysregulation of the Endothelial NO Synthase in Human Endothelial Cells
Accumulating evidence indicates that aldosterone plays a critical role in the mediation of oxidative stress and vascular damage. NADPH oxidase has been recognized as a major source of oxidative stress in vasculature. However, the relation between NADPH oxidase in aldosterone-mediated oxidative stress in endothelial cells remains to be ascertained. The present study aimed to investigate the rel...
متن کاملMicroRNA-155 modulates the proliferation of vascular smooth muscle cells by targeting endothelial nitric oxide synthase.
A variety of microRNAs (miRNAs) have been reported to be significantly be involved in the regulation of vascular smooth muscle cell (VSMC) proliferation, which is an essential process for the formation of atherosclerotic plaque. The objective of the present study was to explore the role of microRNA-155 (miR-155) in the regulation of VSMC growth and migration. A total of 12 atherosclerotic plaqu...
متن کاملذخیره در منابع من
با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید
برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید
ثبت ناماگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید
ورودعنوان ژورنال:
- Molecular medicine reports
دوره 10 1 شماره
صفحات -
تاریخ انتشار 2014