MicroRNA-150 restores endothelial cell function and attenuates vascular remodeling by targeting PTX3 through the NF-κB signaling pathway in mice with acute coronary syndrome
Authors: Xiao-Qing Zhu
Xian-Yuan Luo
Xue-Bin Wang
Ying Li
Wei-Min Ji
Wei Yin
Yi-Shan Ge
Journal: Cell biology international (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: NF-κB signaling pathway; Pentraxin 3; endothelial cell; microRNA-150; vascular remodeling.
Affiliations: Department of Cardiovascular, Suzhou Hospital Affiliated to Nanjing Medical University, Suzhou, 215002, P. R. China., Department of Cardiovascular, Suzhou Science and Technology Town Hospital, Suzhou, 215153, P. R. China.

Abstract:  MicroRNAs (miRNAs) have been known to function as important regulators in the vascular system, with various physiopathological effects such as vascular remodeling and hypertension modulation. We aimed to explore whether microRNA-150 (miR-150) regulates endothelial cell function and vascular remodeling in acute coronary syndrome (ACS), and the involvement of PTX3 and NF-κB signaling pathway. Ten normal mice and sixty ApoE-/- mice were chosen, and their coronary artery tissues and endothelial cells were extracted. ApoE-/- mice were injected with a series of inhibitor or mimic for miR-150, or siRNA against PTX3. The miR-150 expression, NF-κB1, RELA, and PTX3 mRNA expression were assessed by reverse transcription quantitative polymerase chain reaction, and pentraxin-3, p-P50, and p-P65 protein expression by Western blot analysis. Cell viability and migration were assessed by MTT assay and scratch test. Matrigel tube formation assay was employed to determine vascular remodeling of endothelial cells. The dual-luciferase reporter assay verified that PTX3 was a target of miR-150. Mice with ACS presented with decreased miR-150 but increased PTX3. It was observed that the miR-150 mimic and siRNA against PTX3 reduced levels of PTX3, NF-κB1, and RELA in mice, and the miR-150 inhibitor reversed the tendency. The in vitro cell experimentation proved that miR-150 might facilitate endothelial cell proliferation, migration, and restrain vascular remodeling via inhibiting PTX3 expression. On the basis of the results of this study, it was hypothesized that miR-150 could possibly maintain endothelial cell function and suppress vascular remodeling by inhibiting PTX3 through the NF-κB signaling pathway in mice with ACS. 

Retracted: No

PubPeer comments:
 Retracted [14 June 2019] . ----------------------------------- The Editor-in-Chief is retracting this article [1] due to overlap with previously published articles [2, 3]. Fig. 3D u201cmiR-452 mimicsu201d is very similar to Fig. 3D u201csi-BANCRu201d in article [2]. Fig. 3D u201cmiRNCu201d is very similar to Fig. 3E u201csi-NCu201d in article [2] and to Fig. 3E u201cmiR-224 mimicsu201d in article [3]. None of the authors responded to any correspondence from the Editor-in-Chief or publisher regarding this retraction. References - (1). Li R-Z, Wang L-M. Decreased microRNA-452 expression and its prognostic significance in human osteosarcoma. World J Surg Oncol. 2016;14:150. doi: 10.1186 s12957-016-0900-y. - (2). Zhou T, Gao Y. [Increased expression of LncRNA BANCR and its prognostic significance in human hepatocellular carcinoma] . World J Surg Oncol. 2016;14:8. doi: 10.1186 s12957-015-0757-5. [**Expression of Concern**] - (3). Zhu D, Chen H, Yang X, Chen W, Wang L, Xu J, Yu L. [Decreased microRNA-224 and its clinical significance in non-small cell lung cancer patients] . Diagn Pathol. 2014;9:198. doi: 10.1186 s13000-014-0198-4. [**Expression of Concern**] ------------------------------------------ Figure 3: ![] Fig 3 of [Zhao Gao (2016)] [**Retracted**]: ![] For comparison, Figs 3 from [Tang et al (2016)] [**RETRACTED**] and [Lin et al (2014)] [**RETRACTED**]: ![] From Tang et al again, and from [Zhu et al (2014)] [**Expression of Concern**]: ![] Some of this series of retractions was [covered by RetractionWatch] . A broader context is available from [a Chinese science-integrity enthusiast] , blogging in 2016 and citing work by the now-vanished site PlagiarismWatch, to reconstruct a network of **11** mutually-plagiarised papers. All presumably the work of a papermill. ![] ,