Journal of Cellular Physiology最新文献

Chen Y, Mao L, Liu S, Huang S, Lin Q, Zeng M, Huang H, Sun X, Chen H, Huang J, Zhou G, Deng L. The role of TREM-1 in septic myocardial pyroptosis and septic cardiomyopathy in vitro and in vivo. J Cell Physiol. 2024 Dec;239(12):e31445. https://doi.org/10.1002/jcp.31445.

In Figure 5 of “The Role of TREM-1 in Septic Myocardial Pyroptosis and Septic Cardiomyopathy In Vitro and In Vivo,” the authors mistakenly used a scanning electron micrograph from the drug treatment group in Figure 5b (WT control). This has been replaced with the correct control image. The corrected Figure 5 is shown below.

The authors apologize for this error.

The Ribosomal DNA (rDNA) in mammals is organised into large clusters of tandem repeats each of which encodes a single 47S precursor for the 18S, 5.8S, and 28S ribosomal RNAs (rRNAs) that is flanked upstream and downstream by an Intergenic Spacer (IGS) originally referred to as the Non-Transcribed Spacer (NTS). However, in certain cells and under certain environmental conditions the IGS has been found to be transcribed at low level to generate a range of “Noncoding” RNAs (ncRNAs). These ncRNAs have been implicated in the regulation of rRNA synthesis, rDNA silencing and protein sequestration in response to environmental and oncogenic stresses and tumour suppression. Here we review data on the generation, regulation and potential functions of these ncRNAs. We suggest that the majority of the ncRNAs originate from a failure of RNA polymerase I transcription termination by the Reb1- and Myb-related transcriptional “road-block” factor TTF1 and link their expression with tumour suppression.

RETRACTION: X.-H. Gong, H. Liu, S.-J. Wang, S.-W. Liang, and G.-G. Wang, “Exosomes Derived From SDF1-Overexpressing Mesenchymal Stem Cells Inhibit Ischemic Myocardial Cell Apoptosis and Promote Cardiac Endothelial Microvascular Regeneration in Mice With Myocardial Infarction.” Journal of Cellular Physiology 234, no. 8 (2019): 13878–13893. https://doi.org/10.1002/jcp.28070.

The above article, published online on February 5, 2019, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal Editor-in-Chief, Robert Heath, and Wiley Periodicals LLC. A third party shared a report from the National Natural Science Foundation of China, which indicated that data in this article had been purchased from an external company (National Natural Science Foundation of China 2015). An investigation by the publisher found that this fact is not reported in the article and also that the article is missing necessary information on the ethical approval for animal and human experiments performed as part of this study.

The authors responded to an inquiry by the publisher requesting original data and evidence of approval for animal and human experiments. The authors stated that they conducted partial pre-experiments and then commissioned third-party companies to conduct the main experiments. The authors further stated that those companies could not provide raw data. The authors did not provide information regarding ethical approval for the animal and human experiments reported in the article. The authors requested the withdrawal of their article.

The retraction has been agreed to because the data and ethical approval of experiments reported in this article cannot be validated.

While Parkinson′s disease has a multifactorial etiology, 5%–10% of cases present with identifiable disease-causing gene mutations. Further investigation into these mutations is a way to identify underlying pathologic mechanism. One of the rare Parkinson-associated genes is DNAJC13, coding for an endosome-associated protein. Several lines of evidence suggest that disturbed endosomal pathways are instrumental in the development of Parkinson pathology. Recently, we have shown that DNAJC13/RME-8 is a positive modulator of autophagy, a lysosome-associated degradative process. Here, we further characterize the role of the disease-linked DNAJC13(N855S) mutant and perform biochemical, cell biological, co-localization, and expression analysis by employing a newly established cell line with reduced DNAJC13 expression and by transiently expressing the DNAJC13(N855S) mutant variant. We observed that the DNAJC13(N855S) variant is less stable than the wild-type protein and might thus impact proteostasis. Furthermore, the protein has functional deficits as it cannot compensate for the impaired autophagic activity in cells with chronically reduced DNAJC13 levels. In addition, the DNAJC13(N855S) showed a dominant negative effect on the distribution of the cation-independent mannose-6-phosphate receptor without affecting overall cathepsin D levels or activity. Lastly, we observed a decreased expression of several genes related to autophagy induction and biogenesis in stable DNAJC13 knockdown cells. Our data point toward a loss-of-function mechanism of the DNAJC13(N855S) variant and that chronically reduced DNAJC13 protein levels result in a reduced expression of genes largely involved in endosomal traffic and autophagosome biogenesis. The DNAJC13(N855S) mutant might thus cause disease in part by its instability and in part by a dominant negative effect on the autophagic pathway. These data support a pivotal role of endosomal pathway impairment in Parkinson′s disease pathogenesis.

RETRACTION: B. Jin, H. Jin, H.-B. Wu, J.-J. Xu, and B. Li, “Long Non-Coding RNA SNHG15 Promotes CDK14 Expression via miR-486 to Accelerate Non-Small Cell Lung Cancer Cells Progression and Metastasis,” Journal of Cellular Physiology 223, no. 9 (2018): 7164-7172, https://doi.org/10.1002/jcp.26543.

The above article, published online on 06 April 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed upon following an investigation into concerns raised by a third party regarding unrelated flow cytometry panels in Figure 3a showing implausible similarity. The subsequent investigation by the journal team has identified additional concerns regarding inappropriate duplication of image panels between this article (Figure 2D) and two articles published previously by a different group of authors in an unrelated scientific context, depicting different experimental conditions. Therefore, the editors have lost confidence in the data presented and have decided to retract the article. The authors and their affiliated institution were informed about the concerns and the decision to retract, but they remained unresponsive.

Dentinogenesis, the formation of dentin, requires precise coordination of cellular differentiation, extracellular matrix synthesis, and signaling regulation. Here, we elucidate the role of Notum, a secreted Wnt inhibitor, in orchestrating these processes during dentin formation. In Notum^−/− mice, dentin exhibited a thicker yet dysplastic structure with disrupted tubule organization and impaired mineralization, deviating from the functional architecture of healthy dentin. Loss of Notum led to excessive activation of Wnt/β-catenin signaling within the dentin-pulp complex and enhanced expression of odontogenic genes, including dentin sialophosphoprotein (Dspp), and dentin matrix protein 1 (Dmp1). However, this upregulation was uncoupled from proper extracellular matrix composition and mineralization, indicating that initial odontoblast differentiation alone is insufficient for functional dentin formation. At the molecular level, Notum deficiency disrupted matrix integrity, characterized by reduced collagen organization and increased expression of non-collagenous matrix proteins such as bone sialoprotein (Bsp). Collectively, these findings highlight Notum as a critical modulator that fine-tunes Wnt/β-catenin signaling to coordinate cellular differentiation with matrix organization during dentinogenesis. Therapeutic targeting Notum may offer new strategies for restoring dentin integrity and enhancing regenerative outcomes.