Role of ESAT-6 in renal injury by regulating microRNA-155 expression via TLR4/MyD88 signaling pathway in mice with Mycobacterium tuberculosis infection
Authors: Zhong-Qi Zhou
Zhi-Kui Wang
Nan Zhao
Fu-Yun Sun
Yue-Qin Ren
Lei Zhang
Zhong-Wei Ma
Journal: Bioscience Reports (2017)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: Early secretory antigenic target-6; MicroRNA-155; Mycobacterium tuberculosis; Myeloid differentiation factor 88; Renal injury
Affiliations: Department of Nephrology, Linyi People’s Hospital, Linyi 276003, P.R. China, Department of Second Nephrology, Cangzhou Central Hospital, Cangzhou 061000, P.R. China

Abstract:  The study aims to investigate the underlying mechanism involved in the early secretory antigenic target-6 (ESAT-6) in renal injury through regulation of the expression of miR-155 through the oll-like receptor (TLR)-4 (TLR4)/myeloid differentiation factor 88 (MyD88) signaling pathway in Mycobacterium tuberculosis (MTB)-infected mice. Sixty C57BL/6 mice with MTB-induced renal injury were randomly assigned into control, MTB, mimic, inhibitor, inhibitor + ESAT6, and inhibitor + ESAT6 + TAK242 groups. Body weight, the ratio of kidney weight to body weight (Kw/Bw), blood urea nitrogen (BUN), and serum creatinine (Scr) of mice were measured. Flow cytometry was used to detect renal activation in mice. Expressions of miR-155 and ESAT6 were detected by quantitative real-time PCR (qRT-PCR), and Western blotting was used to examine the expressions of ESAT6, TLR4, and MyD88. Expressions of tumor necrosis factor-α (TNF-α), interleukin-17 (IL-17), and interferon-γ (IFN-γ) were measured by qRT-PCR and ELISA. Compared with the control group, the BUN and Scr levels as well as the expression levels of miR-155, TLR4, MyD88, TNF-α, IL-17, and IFN-γ increased, while Kw/Bw decreased in the MTB and mimic groups. In comparison with the MTB group, the above indexes except Kw/Bw were elevated in the mimic group, but were reduced in the inhibitor group, while the Kw/Bw dropped in the mimic group but increased in the inhibitor group. Compared with the inhibitor group, the Kw/Bw decreased while the rest of the indexes increased in the inhibitor + ESAT6 group. ESAT6 may induce renal injury by promoting miR-155 expression through the TLR-4/MyD88 signaling pathway in MTB-infected mice. 

Retracted: Yes

PubPeer comments:
 Checking Figure 2 is enough to conclude that this paper is not worth reading. ![file] , 
 Since the authors are not responding, I checked the manuscript once more. Figure 4A is a total fakery, seen by the repetition of patterns. Just a few examples are shown. ![file] , 
 Fig 5a.  TUNEL staining to observe cardiomyocytes apoptosis in each group . The colored boxes are mine. ![file] , 
 Fig 4b. ![file] It would be easy to spend more time deconstructing these images than the authors spent in constructing them. , 
 Primer discrepancy -at least- for target IL-6. Organisms mentioned in the article = mice, human HEK293 cells ![file] Google scholar results show matches of this primer pair to avian chicken cells ![file] Primer-Blast results from NCBI yield nothing specific for mice and humans ![file] Could the authors explain this? , 
 Retracted [22 February 2022] . ---------- We, the Editors and Publisher of the journal Cell Cycle, have retracted the following article: Xiang Xue Libo Luo (2019) u2018LncRNA HIF1A-AS1 contributes to ventricular remodeling after myocardial ischemia reperfusion injury by adsorption of microRNA-204 to regulating SOCS2 expressionu2019 Cell Cycle, 18:19, https: doi.org 10.1080 15384101.2019.1648960 Since publication, the authors have raised significant concerns about the reliability of the data presented in the article. As the Editor and Publisher also have concerns about the integrity of the reported results, all parties 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 u2018Retractedu2019. ,