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CORRECTION article

Front. Cell Dev. Biol., 13 April 2022
Sec. Cell Death and Survival
Volume 10 - 2022 | https://doi.org/10.3389/fcell.2022.877291

Corrigendum: MicroRNA339 Targeting PDXK Improves Motor Dysfunction and Promotes Neurite Growth in the Remote Cortex Subjected to Spinal Cord Transection

This article is a correction to:

  1. MicroRNA339 Targeting PDXK Improves Motor Dysfunction and Promotes Neurite Growth in the Remote Cortex Subjected to Spinal Cord Transection

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Liu-Lin Xiong,,&#x;Liu-Lin Xiong1,2,3†Yan-Xia Qin&#x;Yan-Xia Qin4†Qiu-Xia Xiao&#x;Qiu-Xia Xiao2†Yuan JinYuan Jin5Mohammed Al-HawwasMohammed Al-Hawwas3Zheng MaZheng Ma5You-Cui WangYou-Cui Wang1Visar Belegu,Visar Belegu6,7Xin-Fu ZhouXin-Fu Zhou3Lu-Lu XueLu-Lu Xue5Ruo-Lan DuRuo-Lan Du1Jia Liu Jia Liu5*Xue Bai Xue Bai2*Ting-Hua Wang,, Ting-Hua Wang1,4,5*
  • 1Institute of Neurobiological Disease, Department of Anesthesiology, Translational Neuroscience Center, West China Hospital, Sichuan University, Chengdu, China
  • 2Animal Zoology Department, Institute of Neuroscience, Kunming Medical University, Kunming, China
  • 3National Traditional Chinese Medicine Clinical Research Base and Western Medicine Translational Medicine Research Center, Department of Cardiac and Cerebral Diseases, Department of Anesthesiology, Affiliated Traditional Chinese Medicine Hospital, Southwest Medical University, Luzhou, China
  • 4School of Pharmacy and Medical Sciences, Sansom Institute, Division of Health Sciences, University of South Australia, Adelaide, SA, Australia
  • 5Department of Histology and Neurobiology, College of Preclinic and Forensic Medicine, Sichuan University, Chengdu, China
  • 6International Center for Spinal Cord Injury, Kennedy Krieger Institute, Baltimore, MD, United States
  • 7Department of Neurology and Pathology, Johns Hopkins University School of Medicine, Baltimore, MD, United States

A Corrigendum on
MicroRNA339 Targeting PDXK Improves Motor Dysfunction and Promotes Neurite Growth in the Remote Cortex Subjected to Spinal Cord Transection

by Xiong, L.-L., Qin, Y.-X., Xiao, Q.-X., Jin, Y., Al-Hawwas, M., Ma, Z., Wang, Y.-C., Belegu, V., Zhou, X.-F., Xue, L.-L., Du, R.-L., Liu, J., Bai, X. and Wang, T.-H. (2020). Front Cell Dev Biol. 8:577. doi:10.3389/fcell.2020.00577

In the original article, there was a mistake in Figure 6A as published. In the original Figure 6A, “there was only sequence of one gRNA, but the sequences of two gRNAs should be provided in the vector map for knocking out microRNA-339, thus we have updated the sequences of two gRNAs in the corrected Figure 6A.” The corrected Figure 6A appears below.

FIGURE 6
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FIGURE 6. The role of miR-339 and its regulatory relationship with PDXK on neurite growth at miR-339 knockout neurons. (A) The construction of vector. (B) Sequencing results: the deleted sequence is black, and the exon sequence is highlighted in blue and red. (C) F1 founder PCR screening: the molecular weight of the wild-type rats is 729 bp; the missing molecular weight of #15, #17, and #21 is 300 bp; the missing molecular weight of #3, #6, and #8 is 202 bp. (D) Electrophoretic band chart for genotype detection. Red green arrow refers to heterozygote rats, yellow arrow refers to wild-type rats, and blue arrow refers to knockout rats. The markers exhibit 100, 250, 500, 750, 1,000, and 2,000 bp, respectively. ± represents heterozygote rats, +/+ represents wild-type rats, and −/− represents the knockout rats. (E) Photomicrographs of neurons detected by Tuj1 staining in Nor, Rea, P-nc, P-si, M-nc and M groups of −/− and +/+ neurons. DAPI counterstaining (blue) demonstrated nuclei of intact cells, and red fluorescence represented Tuj1 positive staining. Apoptotic neurons were determined by Tuj1 and TUNEL staining, presented by Tuj1 + Tunel +/Tuj1 + (%) in Nor, Rea, P-nc, P-si, M-nc and M groups of −/− and +/+ neurons. DAPI counterstaining (blue) demonstrated nuclei of intact cells, red fluorescence represented Tuj1, and red fluorescence represented apoptosis. Scale bar = 50 μm. (F) The length of axon, cell size, cell numbers and apoptosis rate in Nor, Rea, P-nc, P-si, M-nc and M groups of −/−, +/− and +/+ neurons. DAPI counterstaining (blue) demonstrated nuclei of intact cells, red fluorescence represented Tuj1, and red fluorescence represented apoptosis. Scale bar = 50 μm. Data were exhibited as mean ± SD. *p < 0.05 vs. +/+, #p < 0.05 vs. P-nc. Nor, normal; Rea, reagent; P-nc, PDXK-nc; P-si, PDXK-si; M-nc, miR-339-mimic-nc; M, miR-339-mimic; WT, wild type; NC, negative control. −/− represents miR-339 knockout homozygote. +/+ represents wild type. ± represents heterozygote. TUNEL, terminal deoxyribonucleotidyl transferase-mediated dUTP-digoxigenin nick-end labeling; DAPI, 4,6-diamidino-2-phenylindole.

The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.

Publisher’s Note

All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher.

Supplementary Material

The Supplementary Material for this article can be found online at: https://www.frontiersin.org/articles/10.3389/fcell.2020.00577/full#supplementary-material

Supplementary File 1 | The sequence of gRNA1 in the vector map for knocking out microRNA-339.

Supplementary File 2 | The sequence of gRNA2 in the vector map for knocking out microRNA-339.

Keywords: microRNA339, motor cortex plasticity, PDXK, RNA interference, spinal cord injury

Citation: Xiong L-, Qin Y-, Xiao Q-, Jin Y, Al-Hawwas M, Ma Z, Wang Y-, Belegu V, Zhou X-, Xue L-, Du R-, Liu J, Bai X and Wang T- (2022) Corrigendum: MicroRNA339 Targeting PDXK Improves Motor Dysfunction and Promotes Neurite Growth in the Remote Cortex Subjected to Spinal Cord Transection. Front. Cell Dev. Biol. 10:877291. doi: 10.3389/fcell.2022.877291

Received: 16 February 2022; Accepted: 28 February 2022;
Published: 13 April 2022.

Edited and reviewed by:

Uwe Knippschild, University of Ulm, Germany

Copyright © 2022 Xiong, Qin, Xiao, Jin, Al-Hawwas, Ma, Wang, Belegu, Zhou, Xue, Du, Liu, Bai and Wang. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Jia Liu, bGl1amlhYWl4dWV4aUAxMjYuY29t; Xue Bai, Yng3MjQ2QDE2My5jb20=; Ting-Hua Wang, V2FuZ3RoX2VtYWlsQDE2My5jb20=

†These authors have contributed equally to this work

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.