Mechanism of MALAT1 preventing apoptosis of vascular endothelial cells induced by oxygen‚Äìglucose deficiency and reoxidation
Authors: Yuanbo Wu
Guoping Wang
Yuyou Zhu
Journal: Artificial Cells Nanomedicine and Biotechnology (2018)
Discipline: BIOLOGY & BIOCHEMISTRY
Keywords: MALAT1; apoptosis; endothelial cells; oxygen‚Äìglucose deprivation; reoxygenation.
Affiliations: a Department of Neurology , Anhui Provincial Hospital, Anhui Medical University , Hefei , PR China., b Department of Neurology , Anhui Provincial Hospital, The First Affiliated Hospital of University of Science and Technology of China , Hefei , PR China.

Abstract:  Background: Cerebral ischemia/reperfusion (I/R) injury leads to cerebrovascular dysfunction characterized by endothelial cell injury or death. Metastasis-associated lung adenocarcinoma transcript 1(MALAT1) has been reported to be associated with endothelial dysfunction. Our study aimed to investigate the effect of MALAT1 on vascular endothelium. Methods: In this study, oxygen-glucose deprivation and reoxygenation (OGD-R) were used as in vitro studies to investigate the role of MALAT1 in I/R-induced apoptosis of cerebrovascular endothelial cells in an I/R injury model. Primary human brain microvascular endothelial cells were cultured on the condition of OGD-R and MALAT1 expression levels and apoptosis were measured at 6, 9, 12, 24 and 36 h after reoxygenation. The expression of MALAT1 and the apoptosis rate of cells exposed to OGD-R showed the trend of reoxygenation. The kit detected the expression of ROS and PI3K, and the change of Akt signal was detected by Western-blot. Results: After OGD-R, over-expression of MALAT1 lentivirus increased phosphatidylinositol 3-kinase (PI3K) activity and activation of Akt phosphorylation, while decreased apoptosis and caspase 3 activity. Moreover, these effects could be successfully eliminated by treating with a PI3K inhibitor (wortmannin). In contrast, knockdown of MALAT1 lentivirus reduced PI3K activity and Akt phosphorylation, while increased apoptosis and caspase 3 activity. Overexpression or knockdown of MALAT1 had no significant effect on that OGD-R-induced reactive oxygen species (ROS) production. Conclusions: This study first proposed that lncRNA MALAT1 can protect human cerebrovascular endothelial cells from OGD-R-induced apoptosis through a PI3K-dependent mechanism. These findings suggest that MALAT1 may be a potential new therapeutic target for brain I/R injury. 

Retracted: Yes

PubPeer comments:
 As pointed out on Twitter, the figures in this paper bear a striking resemblance to the figures in an older paper by a different set of authors. The older paper is: Jia-Wei Xin and Yu-Gang Jiang, Experimental and Therapeutic Medicine (2017), DOI: 10.3892 etm.2017.4095. Below are the figures from both papers compared to each other. Xin and Jiang (2017) will be shown on the left, and this paper, Wang et al (2018) on the right. First, here are the title pages, showing the similarities in title and abstract:  Figures 1 compared:  The numbering is not completely identical, but here are Figures 2 3 compared:  Figures 4 and 2 compared:  Figures 5 6 and 3 compared:  Figures 7 and 4 AB compared:  Figures 8 and 4 C-F compared:  Could the authors please clarify how they obtained completely identical figures - while working in a completely different research institution? Original Twitter thread: https: twitter.com Samatha_Mathew status 1409208951342649346 , 
 Our study is a joint study of several units, And we worked with Dr. Jiawei Xin from the second Xiangya Hospital in Hunan province. Due to the lack of communication, we submitted the paper to the journal on behalf of our respective units after the paper was completed. At the submission stage, we did not receive any messages from the journal and publishing groups that the duplicate checking was not up to scratch, resulting in repeated publication of the paper. We are deeply sorry for the negative impact we have had on the journal, the publishing company and the readers. We reviewed our academic misconduct sincerely. And we have applied to the journal to retract the paper. , 
 Retracted [3 February 2022] . ----------------------- We, the Editors and Publisher of the journal Artificial Cells, Nanomedicine, and Biotechnology, have retracted the following article: Since publication, the authors repeated some of their experiments and found that under the same conditions they could not repeat the results reported in this paper. In addition, concerns were raised regarding the high degrees of similarity with the following previously published paper: Jia-Wei Xin Yu-gang Jiang (2017) Long noncoding RNA MALAT1 inhibits apoptosis induced by oxygen-glucose deprivation and reoxygenation in human brain microvascular endothelial cells, Experimental and Therapeutic Medicine, 13(4), 1225u20131234, DOI: 10.3892 etm.2017.4095. As this directly impacts the integrity of the reported results and conclusions, the authors alerted the issue to the Editor and Publisher and all have agreed to retract the article to ensure correction of the scholarly record. We have been informed in our decision-making by our policy on publishing ethics and integrity and the COPE guidelines on retractions. The retracted article will remain online to maintain the scholarly record, but it will be digitally watermarked on each page as u201cRetractedu201d. ,