Upregulated microRNA‚Ä?32 rescues cardiac fibrosis and restores cardiocyte proliferation in dilated cardiomyopathy through the phosphatase and tensin homolog‚Äìmediated PI3K/Akt signal transduction pathway
Authors: Jie Lin
Hui Huang
Yu Huang
Chen-Jun Zhang
Ji-De Lu
Zhi-Ru Ge
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: apoptosis; cardiac fibrosis; dilated cardiomyopathy; microRNA-132; phosphatase and tensin homolog
Affiliations: Department of Cardiology, Gongli Hospital, Shanghai, China., Department of Cardiology, Shuguang Hospital, Shanghai University of Traditional Chinese Medicine, Shanghai, China.

Abstract:  Cardiac fibrosis is known to be present in dilated cardiomyopathy (DCM) and it predicts the occurrence of sudden death and congestive heart failure. The aim of our study is to investigate the expression of microRNA-132 (miR-132) and its effect on cardiocyte proliferation, apoptosis, and cardiac fibrosis by binding to phosphatase and tensin homolog (PTEN) through the phosphateidylinositol 3-kinase (PI3K)/protein kinase (Akt) signal transduction pathway in DCM rats. DCM rat models induced by doxorubicin were established and confirmed by an ultrasonic cardiogram. Epithelial cells were treated with inhibitors, activators, and small interfering RNAs to identify the mechanisms by which miR-132 controls cardiocyte activity and cardiac fibrosis. Angiotensin II (Ang II) and aldosterone (ALD) expressions were detected by an enzyme-linked immunosorbent assay. The relationship between PTEN and miR-132 was verified by a dual-luciferase reporter assay. Cell proliferation and apoptosis were tested by the MTT assay and flow cytometry. PTEN was determined to be the target gene of miR-132. Rat models of DCM exhibited a lower level of miR-132, PI3K, Akt, B-cell lymphoma 2, collagen I, and collagen III, but a higher level of PTEN, Bcl-2-associated X protein, and proliferating cell nuclear antigen as well as inflammatory response (Ang II and ALD), accompanied by declined cardiocyte proliferation and elevated apoptosis and cardiac fibrosis. Upregulated miR-132 or silenced PTEN activated the PI3K/Akt pathway, thus facilitating cardiocyte proliferation and repressing cardiocyte apoptosis and cardiac fibrosis, as well as inflammatory responses. Downregulated miR-132 reversed this tendency. These findings indicate that miR-132 activates the PI3K/Akt pathway by inhibiting PTEN expression, thus facilitating cardiocyte proliferation and inhibiting apoptosis and cardiac fibrosis in DCM rats. 

Retracted: Yes

PubPeer comments:
 Fig 3D.  Protein bands of relative protein expressions of PTEN, PI3K, Akt, pu2010Akt, Bclu20102, Bax, collagen I, collagen III, and PCNA in cardiocytes of rats in each group using Western blot analysis .  Resolution is low in the available copy, but I hope readers can see how the loading control (horizontally flipped) resembles the control band seen in a number of other papers within the same genre. E.g. Fig 5B from [Wu et al (2018)] , or 5B from [Wang et al (2018)] , or 6C from [Wen et al (2018)] , and other manifestations linked in that thread.   In general, the protein blobs are like old friends. Here, Figs 2B, 6B, 9B from [Shu et al (2018)] :  , 
 Retracted [19 July 2021] . ---------------------------------------------- The above article, published online on 14 September 2018 in Wiley Online Library has been retracted by agreement between 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. , 
 I am very sorry to see this, but we did had done the experiment all its contents.I just hope it never happens again. , 
 #1 #1 thanks so much for your comments. , 
 #3 #2 I agree and respect opinions of editor in Chief and I will negotiate with him. ,