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Updated: Aug 12, 2025
Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Circ_0007706 downregulation ameliorates neonatal hypoxic ischemic encephalopathy via regulating the miR-579-3p/TRAF6
Jinguang Wang1, Minmin Hua1, Huixin Li2
1Department of Neonatology, The Third Affiliated Hospital of Zhengzhou University, Zhengzhou 450052, China.
Background:
Neonatal hypoxic ischemic encephalopathy (HIE) is a main factor of neonatal death and permanent neurologic deficit. This study sought to investigate the functional role of hsa_circ_0007706 (circ_0007706) in modulating neonatal HIE.
Methods:
In vitro HIE cell model was established in hBMVECs under the condition of oxygen‑glucose deprivation/reperfusion (OGD/R) treatment. qRT-PCR analysis was utilized for detecting the level of circ_0007706, microRNA-579-3p (miR-579-3p) and TNF receptor-associated factor 6 (TRAF6). RNase R treatment and Oligo (dT) 18 primers were employed to verify the features of circ_0007706, and nucleocytoplasmic separation was conducted for determining the location of circ_0007706. CCK-8 assay, EdU assay, and flow cytometry were carried out to measure cell proliferation and apoptosis, respectively. The protein expression of Bax, Bcl-2 and TRAF6 was detected using western blot. Meanwhile, the levels of the pro-inflammatory factors were determined via ELISA. SOD activity and MDA level were assessed via the respective kits. Besides, dual-luciferase reporter assay and RNA pull-down were used to identify the association between miR-579-3p and circ_0007706 or TRAF6.
Results:
Circ_0007706 was elevated in HIE newborns and OGD/R cell model. Knockdown of circ_0007706 greatly alleviated OGD/R-induced injury, inflammatory response and oxidative stress. We found that miR-579-3p was a direct target of circ_0007706, and miR-579-3p inhibitor could reverse the impact of circ_0007706 knockdown on OGD/R-caused cell damage in hBMVECs. In addition, miR-579-3p directly interacted with TRAF6, and the protective effects of miR-579-3p on OGD/R-induced injury in hBMVECs were harbored by TRAF6 overexpression. Our data indicated that circ_0007706 knockdown could downregulate the expression of TRAF6 by sponging miR-579-3p in OGD/R-treated hBMVECs.
Conclusion:
This study demonstrated that circ_0007706 knockdown assuaged HIE-induced injury by decreasing TRAF6 expression via targeting miR-579-3p.
