Retracted : microRNA‚Ä?42‚Ä?p protects against acute lung injury in mice with severe acute pancreatitis by suppressing the mitogen‚Äêactivated protein kinase signaling pathway through the negative regulation of P21‚Äêactivated kinase 1
Authors: Xing-Mao Wu
Bin Zang
Jia Jia
Yang Zhao
Kai-Qiang Ji
Hai-Yuan Wang
Xiao-Peng Gao
Journal: Journal of Cellular Biochemistry (2019)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: P21-activated kinase 1 (PAK1); acute lung injury (ALI); microRNA-542-5p; mitogen-activated protein kinase (MAPK) signaling pathway; severe acute pancreatitis.
Affiliations: Intensive Care Unit, Shengjing Hospital, China Medical University, Shenyang, China.

Abstract:  Severe acute pancreatitis (SAP) is a condition associated with high rates of mortality and lengthy hospital stays. In the current study, SAP mouse models were established in BALB/c wild-type and P21-activated kinase 1 (PAK1) knockdown mice with the objective of determining the expression of microRNA-542-5p (miR-542-5p) and the subsequent elucidation of the mechanism by which it influences acute lung injury (ALI) by mediating mitogen-activated protein kinase (MAPK) signaling and binding to PAK1. The targeting relationship between miR-542-5p and PAK1 was verified using the bioinformatics prediction website and by the means of a dual-luciferase reporter assay. Following the SAP model establishment, the mice were assigned into various groups with the introduction of different mimic and inhibitors in an attempt to investigate the effects involved with miR-542-5p on inflammatory reactions among mice with SAP-associated ALI. Our results indicated that PAK1 was targeted and negatively mediated by miR-542-5p. Mice with SAP-associated ALI exhibited an increased wet-to-dry weight ratio, myeloperoxidase activity, serum amylase activity, TNF-Œ±, interleukin-1 beta (IL-1Œ≤), and intercellular adhesion molecule-1 (ICAM-1) contents, p-p38MAPK, p-ERK1/2, and p-JNK protein levels as well as PAK1 positive expression, while decreased miR-542-5p levels were observed. Functionally, overexpression of miR-542-5p improves ALI in mice with SAP via inhibition of the MAPK signaling pathway by binding to PAK1.Based on the evidence from experimental models, miR-542-5p was shown to improve ALI among mice with SAP, while suggesting that the effect may be related to the inactivation of the MAPK signaling pathway and downregulation of PAK1 gene. Thus, miR-542-5p could serve as a promising target for ALI treatment. 

Retracted: Yes

PubPeer comments:
 Fig 4A ( on the basis of HE staining results of pancreas (u00d7400, scale = 25 u00b5m), pancreas in the miRu2010542u20105p mimic, PAK1 KD and miRu2010542u20105p inhibitor+PAK1 KD groups has slight edema with little inflammation cell infiltration. The overall pathological change is significantly better than that in the SAP group ) and B ( on the basis of HE staining results of lung tissues (u00d7400, scale = 25 u00b5m), The pulmonary interstitium in the miRu2010542u20105p mimic, PAK1 KD and miRu2010542u20105p inhibitor+PAK1 KD groups appears slight edema, and inflammatory cell infiltration, alveolar septal widening, and local hemorrhage thickening in those three groups have significant improvement when compared with the SAP group ).  For comparison, Fig 1H and 3E from [Wu et al (2018)] ,  HE staining (200u00d7) of pancreas and lung and  HE staining (200u00d7) of pancreas and lung according to Schmidt scoring system   Could the authors comment on the similarities? The matching figures seem to represent different treatments. , 
 Fig 9A.  protein bands of ERK1 2, JNK and p38MAPK .  The loading control is suggestive of a papermill contribution to this paper, as it features in a large number of other papers by otherwise-unrelated teams of researchers. Picking two example at random: Fig 8A from [Wu et al (2018)] , Fig 3C of [Luo et al (2018)] :   Many more examples in that thread, and in a Google document: https: docs.google.com spreadsheets d 1r0MyIYpagBc58BRF9c3luWNlCX8VUvUuPyYYXzxWvgY edit?usp=sharing , 
 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. As several flaws and inconsistencies between results presented and experimental methods described were found, the editors consider the conclusions of this article to be invalid. ,