Retraction : miR‐200a mediates protection of thymosin β4 in cardiac microvascular endothelial cells as a novel mechanism under hypoxia‐reoxygenation injury
Authors: Xiping Liu
Bo Yu
Xiaolong Zhu
Yang Li
Aolin Du
Journal: Journal of Cellular Biochemistry (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Myocardial ischemia/reperfusion injury; Thymosin beta-4; cardiac microvascular endothelial cells; nuclear factor erythroid 2-related factor 2.
Affiliations: Department of Cardiology, The First Affiliated Hospital of China Medical University, Shenyang 110001, Liaoning, PR China.

Abstract:  Thymosin beta-4 (Tβ4) is a ubiquitous protein, which has been suggested to regulate multiple cell signal pathways and a variety of cellular functions. However, the role Tβ4 plays in the cardiac microvascular endothelial cells (CMECs) under myocardial ischemia/reperfusion injury (MIRI) is currently unknown. Here we investigated the effects of Tβ4 on hypoxia/reoxygenation (H/R) induced CMECs injury and its potential molecular mechanism. Cultured CMECs were positively identified by flow cytometry using antibody against CD31 and VWF/Factor VIII, which are constitutively expressed on the surface of CMECs. Then the reduced level of Tβ4 was detected in H/R-CMECs by RT-qPCR. In order to determine the effects of Tβ4 on H/R-CMECs, we transfected the overexpression or silence vector of Tβ4 into CMECs under H/R condition. Our results indicated that H/R treatment could reduce proliferation, increased apoptosis, adhesion and ROS production in CMECs, which were attenuated by Tβ4 overexpression or aggravated by Tβ4 silence, implying Tβ4 is able to promote CMECs against H/R-induced cell injury. Furthermore, the microRNA 200a (miR-200a) level was also increased by Tβ4 in H/R-CMECs or reduced by Tβ4 siRNA. To investigated the mechanism of protective effects of Tβ4 on CMECs injury, the miR-200a inhibitor was transfected into H/R-CMECs. The results indicated that inhibition of miR-200a inversed the protection of Tβ4 on H/R-CMECs, specifically including cell proliferation, cell adhesion, cell apoptosis and ROS production, as well as nuclear factor erythroid 2-related factor 2 (Nrf2) nuclear translocation. In conclusion, our results determined that Tβ4 attenuated H/R induced CMECs injury by miR-200a-Nrf2 signaling. This article is protected by copyright. All rights reserved. 

Retracted: No

PubPeer comments:
 Retracted Withdrawn: The above article, from Journal of Cellular Biochemistry, u201cmiRu2010200a mediates protection of thymosin u03b24 in cardiac microvascular endothelial cells as a novel mechanism under hypoxiau2010reoxygenation injuryu201d by Yang Li, Xiaolong Zhu, Xiping Liu, Aolin Du, and Bo Yu published online on 31 August 2017 in Wiley Online Library , has been withdrawn by agreement between the journal Editor in Chief Gary S. Stein and John Wiley and Sons, Inc. The retraction has been agreed because the authors are not responding to requests to finalize their article for publication in the journal as the Version of Record. Meanwhile, there s Fig 2A.  Tu03b24 inhibited the cell apoptosis of H R-induced CMECs. (A) Cell apoptosis was detected by flow cytometry . ![file] Through inexplicable coincidence, the plots marked with blue and brown rectangles are recognisable versions of panels in Fig 3A of [Long et al (2017)] . ![file] ... and in Fig 2G from [Li et al (2018)] . ![file] ,