PRR34‐AS1 overexpression promotes protection of propofol pretreatment against ischemia/reperfusion injury in a mouse model after total knee arthroplasty via blockade of the JAK1‐dependent JAK‐STAT signaling pathway
Authors: Ren Liao
Jian-Ping Zhang
Ru-Rong Wang
Quan-Yun Wang
Peng-Cheng Zheng
Miao Yang
Hua Fang
Hua-Feng Li
Fang-Xiang Zhang
Journal: Journal of Cellular Physiology (2020)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: JAK-STAT signaling pathway; JAK1; PRR34-AS1; apoptosis; ischemia/reperfusion injury
Affiliations: Department of Anesthesiology, Guizhou Provincial People's Hospital, Guiyang, China., Department of Anesthesiology, Guizhou University People's Hospital, Guiyang, China., Department of Anesthesiology, West China Second University Hospital, Sichuan University, Chengdu, China., Department of Anesthesiology, West China Hospital, Sichuan University, Chengdu, China., Guizhou University Research Center for Analysis of Drugs and Metabolites, Guizhou University, Guiyang, China.

Abstract:  Long noncoding RNAs have been documented to be protective against ischemia/reperfusion (I/R) injury. However, few research works have focused on the protective effects of PRR34-AS1 on I/R injury after total knee arthroplasty (TKA). The objective of the present study was to investigate the possible effect of PRR34-AS1 on I/R injury after TKA. A mouse model with I/R injury after TKA was established. The interaction between PRR34-AS1 and Janus kinase 1 (JAK1) was examined and thoroughly investigated. Next, the effects of PRR34-AS1 on the expression of apoptosis-related proteins, JAS-signal transducer and activator of transcription (STAT) signaling pathways, and inflammation-related genes, chondrocyte proliferation, and apoptosis were analyzed after gain- and loss-of-function experiments. Attenuated symptoms were observed in mice pretreated with propofol, which was evidenced by decreased positive expression rate of JAK1 protein and superoxide dismutase content along with increased malondialdehyde content and IL-10 levels. PRR34-AS1 was poorly expressed in mice with I/R injury after TKA. JAK1 was a target of PRR34-AS1. Upregulated PRR34-AS1 diminished expression of JAK1, STAT1, JAK2, and STAT3 as well as cell apoptosis, while enhancing cell proliferation in vitro. Furthermore, JAK1 silencing could reverse the suppressed cell proliferation and enhanced cell apoptosis of chondrocytes imposed by silencing PRR34-AS1. Upregulation of PRR34-AS1 can potentially relieve I/R injury after TKA in mice pretreated with propofol through inhibition of the JAS-STAT signaling pathway by targeting JAK1. 

Retracted: No

PubPeer comments:
 Tables 2 and 3 show the level of several enzymes, cytokines, etc. as measured in 12 mice per group. The tables list a total of 18 mean values (mean of 12 mice) and the standard deviation (SD). The SDs are all small. Measured as the percentage of the mean value they belong to, almost all (17 18 values) fall between 7-10%. Here is a plot of the narrow distribution of these values. ![file] Could that authors please provide the raw data from these measurements (ELISA or whatever was used)? , 
 The Western blots in Figures 3C and 5C all show very regularly spaced bands without any background staining, except for flame-like protrusions around each band. Could the authors please show the original, uncropped blots? ![file] , 
 I compiled this montage of Western Blots, sourced from various papers, each with its own PP thread. To my mind there is (as it were) a family kinship among them all, all sampling a small corner of  morphological space . Many other family members could be adduced. Clockwise from upper left: - [Wang et al (2020)] - [Gao et al (2021)] - [Chen et al (2020)] - [He et al (2021)] . ![file] In addition, WBs from [Lv et al (2020)] *[retracted]* ![] This may be my over-active imagination, but the WBs in the present paper seems to fit into the same genre. , 
 Fig 7:  Flow cytometry analysis of PIu2010stained cells at G0 G1, S, and G2 M phases . ![file] These plots appear to be hand-drawn. The G0 G1, S and G2 M contributions do not add up the way they should. ,