Retracted : Effects of microrna‚Ä?3 on mouse cardiac microvascular endothelial cells injury and inflammatory response by mediating SPP1 through the NF‚ÄêŒöB pathway
Authors: Zhi-Feng Bai
Su-Xia Ma
Wei Wang
Hui-Ying Wu
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: MicroRNA-93 (miR-93); NF-Œ∫B signaling pathway; SPP1; cardiac microvascular endothelial cells; inflammatory response
Affiliations: Second Department of Cardiovascular Medicine The First People‚Äôs Hospital of Shangqiu City Shangqiu China, Department of Cardiovascular Medicine Fuwai Cardiovascular Hospital Beijing China, Department of General Medicine Henan Provincial People‚Äôs Hospital Zhengzhou China

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-Œ∫B signaling pathway. Methods: Healthy Balb/c mice were recruited to establish a mouse model with myocarditis using the CVB3 virus. Mice were grouped into normal, blank, negative control (NC), miR-93 inhibitor, miR-93 mimic, SPP1 short hairpin RNA (shRNA), and miR-93 mimic+SPP1 shRNA groups. Reverse transcription quantitative polymerase chain reaction and Western blot analysis were applied 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/propidium iodide double staining was conducted to examine cell apoptosis, enzyme-linked immunosorbent assay was conducted to measure secretion of inflammatory factors, and chemical colorimetry was conducted 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: Taking our results together, we conclude that upregulation of miR-93 reduces CMECs injury and inflammatory response by negatively targeting SPP1 via inactivating the NF-Œ∫B signaling pathway. 

Retracted: Yes

PubPeer comments:
 Fig 7A.  Cell apoptosis rate of CMECs in each group by Annexin V-FITC PI double staining . All seven flow-cytometry plots have the same group of cells in the centre. Other clusters of shared cells are visible.  , 
 Fig 5a.  Expressions of SPP1, p50, p65, VEGFA, Bax and Bcl-2 in each group by western blotting Notes: A, electrophoresis of related proteins in each group .  For comparison, Fig. 4A. and Fig. 7C from [Long et al (2018)] .  Other manifestations listed [here] . , 
 Retracted [30 June 2021] . ----------------------------------- The above article, published online on 12 December 2017 in Wiley Online Library has been retracted by agreement between the the journal s Editor in Chief, Prof. Dr. Christian Behl, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. A detailed investigation revealed that several image elements of the experimental data were published elsewhere in a different scientific context. Thus, the editors consider the conclusions of this article to be invalid. ,