Retracted : Effects of microRNA‐10a on synapse remodeling in hippocampal neurons and neuronal cell proliferation and apoptosis through the BDNF‐TrkB signaling pathway in a rat model of Alzheimer's disease
Authors: Mi-Shan Wu
Jin-Dong Guo
Bo-Wen Wu
Journal: Journal of Cellular Physiology (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Alzheimer's disease; BDNF-TrkB; apoptosis; microRNA-10a; neuronal cell
Affiliations: Department of Formulas, Basic Medicine College, Hebei University of Chinese Medicine, Shijiazhuang, P. R. China., Hebei Key Laboratory of Chinese Medicine Research on Cardio-Cerebrovascular Disease, Shijiazhuang, P. R. China.

Abstract:  The aim of this study was to research the effects of microRNA-10a (miR-10a) on synapse remodeling and neuronal cells in rats with Alzheimer's disease (AD) through BDNF-TrkB signaling pathway. Rat models of AD were established. The neuronal cells were allocated into blank, negative control (NC), miR-10a mimics, miR-10a inhibitors, K252a, and miR-10a inhibitors + K252a groups. Expressions of miR-10a, p38, PSD95, BDNF, cAMP-response element-binding protein (CREB), and tropomyosin receptor kinase B (TrκB) were tested using RT-qPCR and Western blotting. Neuron cell proliferation, cycle, and apoptosis were observed using Cell counting kit-8 (CCK8) assay and flow cytometry. The ultrastructure was observed under a scanning electron microscope. The miR-10a expression of AD rats increased while p38, PSD95, BDNF, CREB, and TrκB expression decreased compared with the normal rats. Dual luciferase reporter gene assay testified miR-10a targeted BDNF. The expressions of p38, PSD95, BDNF, CREB, and TrκB decreased in the miR-10a mimics and K252a groups. Compared with the blank and NC group, the miR-10a mimics and K252a groups showed inhibited cell growth rate with cells mainly rest in the G1 satge, and increased spoptosis. The miR-10a inhibitors group presented an opposite trend to the miR-10a mimics and K252a groups. The synapse was complete and abundant in the miR-10a inhibitors group while disappeared in the miR-10a mimics and K252a groups. The results indicated that miR-10a restrains synapse remodeling and neuronal cell proliferation while promoting apoptosis in AD rats via inhibiting BDNF-TrkB signaling pathway. 

Retracted: Yes

PubPeer comments:
 Fig 9A.  Neuronal cell cycles in CA3 region of AD rat hippocampus after transfection for 48 h Note: A, the results of flow cytometry . The authors evidently coaxed neurons sourced from adult rat hippocampus tissue back into a stem-cell state whereby they could undergo mitosis and proliferate. This sounds like a remarkable discovery and I am puzzled that the authors are so off-hand about it. ![file] Anyway, the raw cell-count data in three of these flow-cytometry plots are remarkably similar to results published in otherwise-unrelated papers (although the results of fitting these histograms with G0 G1, G2, So templates are different). Fig. 10A from [Zhang et al (2018)] .  The cycle distribution of cardiomyocytes in each group after transfection. Notes: A, Flow cytometry . ![] Fig. 9A,C from [Qian et al (2018)] .  Cycle distribution of pancreatic cancer and PANC-1 cells in each group. Note: A, pancreatic cancer cell cycle distribution in each group... C, PANC-1 cell cycle distribution in each group . ![] , 
  Fig 10 Apoptosis rate of neuronal cells in CA3 region of AD rat hippocampus after transfection for 48 h . ![file] For comparison, Fig 6 of [Ao et al (2017)] . ![file] The arrangements of points in corresponding panels is clearly not identical (the resolutions are different, for instance), but they are also more similar in an impressionist way than chance would lead us to expect. It is as if one set of panels provided the model for the other. I can only suppose that Sheldrake s Morphogenetic Field was involved somehow. , 
 Retracted [30 June 2021] . ----------------------- The above article, published online on 07 December 2017 in Wiley Online Library has been retracted by agreement between the journal s Editor in Chief, Prof. Dr. Gregg Fields, and Wiley Periodicals LLC. The retraction has been agreed following an investigation based on allegations raised by a third party. Several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. ,