Apolipoprotein A1 and heterogeneous nuclear ribonucleoprotein E1 implicated in the regulation of embryo implantation by inhibiting lipid peroxidation

• Published in: Reproductive biomedicine online Vol. 33; no. 5; pp. 635 - 645
• Main Authors: Jia, Jia, Gou, Jinhai, Zhao, Xia, Yi, Tao, Li, Zhengyu
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier Ltd 01.11.2016
• Subjects: Animals; Apolipoprotein A-I - genetics; Apolipoprotein A-I - physiology; apolipoprotein A1; embryo implantation; Embryo Implantation - genetics; Endometrium - metabolism; Female; Gene Expression Regulation, Developmental; Gene Knockdown Techniques; heterogeneous nuclear ribonucleoprotein E1; Heterogeneous-Nuclear Ribonucleoproteins - genetics; Heterogeneous-Nuclear Ribonucleoproteins - physiology; lipid peroxidation; Lipid Peroxidation - genetics; Male; Malondialdehyde - metabolism; Mice; Mice, Inbred C57BL; Nitric Oxide Synthase Type III - genetics; Nitric Oxide Synthase Type III - metabolism; Obstetrics and Gynecology; Reverse Transcriptase Polymerase Chain Reaction; RNA Interference; Superoxide Dismutase - metabolism; apolipoprotein A1; heterogeneous nuclear ribonucleoprotein E1; lipid peroxidation; embryo implantation
• ISSN: 1472-6483; 1472-6491
• DOI: 10.1016/j.rbmo.2016.07.011

Abstract It is known that apolipoprotein A1 (apoA1) is a stimulator of endothelial nitric oxide synthase (eNOS), and that heterogeneous nuclear ribonucleoprotein E1 (hnRNP-E1)-containing RNP complexes is a key protector of basal stabilization of eNOS mRNA. Recently, we found that apoA1 and hnRNP-E1 were up-regulated during peri-implantation period, and the purpose of this study was to explore the roles of apoA1 and hnRNP-E1 during this period in the mouse. It was found that the up-regulation of apoA1 and hnRNP-E1 were dependent on the presence and status of blastocysts, on endometrial decidualization and on the progesterone and 17β-oestradiol status. Knockdown of apoA1 or hnRNP-E1 both resulted in reduced numbers of embryo implantations and neonates ( P < 0.01), and lipid peroxidation was found to be involved. On pregnancy day 5 eNOS expression and superoxidase dismutase (SOD) quantity were increased, and malondialdehyde (MDA) quantity was decreased at implantation sites. The knockdown of either apoA1 or hnRNP-E1 led to down-regulation of eNOS ( P < 0.01) and to an increase in the quantity of MDA ( P < 0.05), and a decrease in the amount of SOD ( P < 0.01). These findings suggest that apoA1 and hnRNP-E1 may play roles in embryo implantation by inhibiting lipid peroxidation.