Retracted : Microrna‐139‐5p inhibits epithelial‐mesenchymal transition and fibrosis in post‐menopausal women with interstitial cystitis by targeting LPAR4 via the PI3K/Akt signaling pathway
Authors: Yin-Jun Gu
Wei-Lin Fang
Qi-Bo Fu
Wei Xue
Dong-Ming Liu
Chen Jiang
Zhen Tong
Ting-Ting Lv
Jian-Wei Lv
Journal: Journal of Cellular Biochemistry (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: LPAR4; PI3K/AKT signaling pathway; epithelial-mesenchymal transition; fibrosis; interstitial cystitis
Affiliations: Department of Urology, South Campus, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, P. R. China., Department of Urology, Renji Hospital, School of Medicine, Shanghai Jiaotong University, Shanghai, P. R. China.

Abstract:  The study explores whether miR-139-5p targeting LPAR4 affects epithelial-mesenchymal transition (EMT) and fibrosis in post-menopausal women with interstitial cystitis (IC) via the PI3K/Akt signaling pathway. Bladder tissues of IC and normal bladder tissues were collected. The pathology of bladder tissues was observed by HE, Masson and Picrosirius red staining. LPAR4 positive expression rate were determined by IHC. ELISA was performed to detect the levels of IL-6, IL-8, IL-10, and TNF-α. Rat IC models were randomized into seven different groups. miR-139-5p, LPAR1, LPAR2, LPAR3, LPAR4, LPAR5, P13K, Akt, E-cadherin, N-cadherin, Vimentin, TGF-β1, and CTGF expression were determined by RT-qPCR and Western blotting. Dual luciferase reporter gene assay verified that LPAR4 is a target gene of miR-139-5p. Fibrosis was a pathological manifestation of IC. The IC group showed higher LPAR4, PI3K, Akt, p-PI3K, p-Akt, N-cadherin, Vimentin, TGF-β1, and CTGF expression but lower miR-139-5p and E-cadherin expression than the normal group. The levels of IL-6, IL-8, IL-10, and TNF-α expression decreased while HB-EGF increased in the IC group in comparison of the normal group. Compared with the blank and NC groups, E-cadherin expression was increased in the miR-139-5p mimic and siRNA-LPAR4 groups, while LPAR4, PI3K, Akt, p-P13K, p-Akt, N-cadherin, Vimentin, TGF-β1, and CTGF expression were decreased. An opposite trend was found in the miR-139-5p inhibitor group. The miR-139-5p decreased in the miR-139-5p inhibitor + siRNA-LPAR4 and miR-139-5p inhibitor + wortmannin groups. Conclusively, miR-139-5p targeting LPAR4 inhibits EMT and fibrosis in post-menopausal IC women through the PI3K/Akt signaling pathway. 

Retracted: Yes

PubPeer comments:
 *[right]* Fig. 3C.  The miR-139-5p, LPAR1, LPAR2, LPAR3, LPAR4, LPAR5, PI3K, Akt, E-cadherin, N-cadherin, Vimentin, TGF-u03b21 and CTGF mRNA and protein expressions in the IC group and the normal group ... C, image for Western blotting; D, LPAR1, LPAR2, LPAR3, LPAR4 and LPAR5 protein expressions . *[left]* Figure 7C from [Lu et al (2018)] .  Expressions of miR-708, BAMBI, Wnt10B, P53, Bcl-2, VEGF, Fas, Bax, Caspase-3, and cleaved Caspase-3 after transfection in each group.... C, electrophoretograms of protein expressions . ![file] No authors in common. How to explain the resemblance within the loading controls? Now comparing 7C from Lu et al with the present 6C. The resolution is not high but enough to see that the loading control bands are the same. ![file] , 
 #2 Fig 6C again, and 67 of Lu et al (2018): ![] Another sighting of the loading control, this time labeled as beta-Actin rather than as GAPDH. Fig 8A from [Wu et al (2018)] . ![] , 
 Retracted [30 June 2021] . ------------------------------------- The above article, published online on 14 December 2017 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. ,