Publication Date:
2017-12-13
Description:
ABSTRACT Background: This study aims to investigate the regulative role of microRNA-93 (miR-93) in mouse cardiac microvascular endothelial cells (CMECs) injury and inflammatory response by negatively targeting SPP1 gene via the NF-κB signaling pathway. Methods: Healthy Balb/c mice were recruited to establish mouse model with myocarditis using CVB3 virus. Mice were grouped into the normal, blank, negative control (NC), miR-93 inhibitor, miR-93 mimic, SPP1 shRNA and miR-93 mimic + SPP1 shRNA groups. RT-qPCR and western blotting were applied respectively to determine the expressions of miR-93, SPP1, VEGFA, p50, p65, Bax and Bcl-2. MTT assay was conducted to evaluate cell viability, Annexin V-fluorescein isothiocyanate (FITC)/propidium iodide (PI) double staining to examine cell apoptosis, ELISA to measure secretion of inflammatory factors, and chemical colorimetry to determine NO secretion. Results: SPP1 was a target gene of miR-93. Compared with the normal group, other six groups showed increased expressions of SPP1, p50, p65, VEGFA and Bax as well as cell apoptosis rate and secretion of cell inflammatory factors, and decreased expression of Bcl-2, cell viability and NO secretion. Compared with the blank group, the miR-93 inhibitor group showed elevated expressions of SPP1, p50, p65, VEGFA and Bax as well as cell apoptosis rate and secretion of cell inflammatory factors, and reduced Bcl-2, cell viability and NO secretion. While the miR-93 mimic and SPP1 shRNA groups displayed opposite results. Conclusion: Taken together, we conclude that up-regulation of miR-93 reduces CMECs injury and inflammatory response by negatively targeting SPP1 via inactivating the NF-κB signaling pathway. This article is protected by copyright. All rights reserved
Electronic ISSN:
0091-7419
Topics:
Biology
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Chemistry and Pharmacology
,
Medicine
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