Corrigendum: MiR-136-5p/FZD4 Axis Is Critical for Wnt Signaling-Mediated Myogenesis and Skeletal Muscle Regeneration

IF 4.5 2区 生物学 Q2 CELL BIOLOGY
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引用次数: 0

Abstract

This article corrects the following:

miR-136-5p/FZD4 axis is critical for Wnt signaling-mediated myogenesis and skeletal muscle regeneration

Zhang, Donghao, Lingqian Yin, Zhongzhen Lin, Chunlin Yu, Jingjing Li, Peng Ren, Chaowu Yang, Mohan Qiu, and Yiping Liu

Journal of Cellular Physiology

https://doi.org/10.1002/jcp.31046

First published online: 23 May 2023

Correction text:

A reviewer alerted the publisher that an earlier version of the revised manuscript had mistakenly been published in place of the accepted version of the article. This error occurred accidentally during the production process. We apologize for the error and any inconvenience that may have arisen as a result. The following changes align with the final accepted version of the article.

Figure 1F has been updated to include MyHC and Hoechst immunofluorescence staining of C2C12 at different stages. The corrected Figure 1 and associated legend are as follows:

The layout of Figure 4 has been changed to improve the visibility of the images of the cells in panels A and G. In addition, the MyoG Western blot image in panel E has been changed. The corrected Figure 4 and associated legend are as follows:

The Bcl+antagomir ZsGreen panel in Figure 5F has been replaced, and the title of the figure has been updated to accurately reflect that FZD4 expression attenuates antagomiR-136-5p-mediated muscle regeneration after injury. The corrected Figure 5 and associated legend are as follows:

Finally, the missing Supplemental Figure 1 has been added as follows:

Figure S1. FZD4 promotes differentiation of C2C12 cells in vitro.

(A) Expression levels of PCNA, CDK2, MyoD and MyoG mRNA in C2C12 cells after overexpression of FZD4 (n = 9 cultures; mean ± SEM). (B) Western blot analysis analysis of the PCNA and MyoG protein levels in C2C12 cells. β-Tubulin was used as an internal reference. (C) EdU and Hoechst (nuclei) staining analysis. The scale bar represents 100 μm. (D) Fold change of proliferation rate of C2C12 cells in each group (n = 6 cultures; mean ± SEM). EdU (red), Hoechst (blue). *p < 0.05, **p < 0.01, ***p < 0.001.

Abstract Image

更正:MiR-136-5p/FZD4轴对Wnt信号介导的肌肉发生和骨骼肌再生至关重要。
miR-136-5p/FZD4轴对Wnt信号介导的肌肉发生和骨骼肌再生至关重要张,郝东,尹凌倩,林忠珍,于春林,李晶晶,任鹏,杨朝武,邱默涵,刘一平,细胞生理学杂志https://doi.org/10.1002/jcp.31046First在线发表:2023年5月23日更正文本:一位审稿人提醒出版商,修改后的手稿的早期版本错误地取代了文章的接受版本。这个错误是在生产过程中意外发生的。我们对这个错误和由此产生的任何不便表示歉意。以下更改与文章的最终接受版本一致。图1F已更新,纳入了不同阶段C2C12的MyHC和Hoechst免疫荧光染色。更正后的图1和相关图例如下:图4的布局已被更改,以提高A和g组细胞图像的可视性。此外,E组的MyoG Western blot图像已被更改。更正后的图4及相关图例如下:图5F中的Bcl+antagomir ZsGreen面板已被替换,图标题已更新,以准确反映FZD4表达减弱antagomir -136-5p介导的损伤后肌肉再生。更正后的图5和相关图例如下:最后,将缺失的补充图1添加如下:图S1。(A)过表达FZD4后C2C12细胞中PCNA、CDK2、MyoD和MyoG mRNA的表达水平(n = 9个培养;平均值±SEM)。(B) C2C12细胞PCNA和MyoG蛋白水平的Western blot分析。以β-微管蛋白为内参。(C) EdU和Hoechst(核)染色分析。比例尺代表100 μm。(D)各组C2C12细胞增殖率的倍数变化(n = 6个培养;平均值±SEM)。EdU(红色),Hoechst(蓝色)。*p < 0.05, **p < 0.01, **p < 0.001。
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来源期刊
CiteScore
14.70
自引率
0.00%
发文量
256
审稿时长
1 months
期刊介绍: The Journal of Cellular Physiology publishes reports of high biological significance in areas of eukaryotic cell biology and physiology, focusing on those articles that adopt a molecular mechanistic approach to investigate cell structure and function. There is appreciation for the application of cellular, biochemical, molecular and in vivo genetic approaches, as well as the power of genomics, proteomics, bioinformatics and systems biology. In particular, the Journal encourages submission of high-interest papers investigating the genetic and epigenetic regulation of proliferation and phenotype as well as cell fate and lineage commitment by growth factors, cytokines and their cognate receptors and signal transduction pathways that influence the expression, integration and activities of these physiological mediators. Similarly, the Journal encourages submission of manuscripts exploring the regulation of growth and differentiation by cell adhesion molecules in addition to the interplay between these processes and those induced by growth factors and cytokines. Studies on the genes and processes that regulate cell cycle progression and phase transition in eukaryotic cells, and the mechanisms that determine whether cells enter quiescence, proliferate or undergo apoptosis are also welcomed. Submission of papers that address contributions of the extracellular matrix to cellular phenotypes and physiological control as well as regulatory mechanisms governing fertilization, embryogenesis, gametogenesis, cell fate, lineage commitment, differentiation, development and dynamic parameters of cell motility are encouraged. Finally, the investigation of stem cells and changes that differentiate cancer cells from normal cells including studies on the properties and functions of oncogenes and tumor suppressor genes will remain as one of the major interests of the Journal.
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