Journal of cellular biochemistry最新文献

Mammals exhibit two distinct types of adipose depots: white adipose tissue (WAT) and brown adipose tissue (BAT). While WAT primarily functions as a site for energy storage, BAT serves as a thermogenic tissue that utilizes energy and glucose consumption to regulate core body temperature. Under specific stimuli such as exercise, cold exposure, and drug treatment, white adipocytes possess a remarkable ability to undergo transdifferentiation into brown-like cells known as beige adipocytes. This transformation process, known as the “browning of WAT,” leads to the acquisition of new morphological and physiological characteristics by white adipocytes. We investigated the potential role of Irisin, a 12 kDa myokine that is secreted in mice and humans by skeletal muscle after physical activity, in inducing the browning process in mesenchymal stromal cells (MSCs). A subset of the MSCs possesses the remarkable capability to differentiate into different cell types such as adipocytes, osteocytes, and chondrocytes. Consequently, comprehending the effects of Irisin on MSC biology becomes a crucial factor in investigating antiobesity medications. In our study, the primary objective is to evaluate the impact of Irisin on various cell types engaged in distinct stages of the differentiation process, including stem cells, committed precursors, and preadipocytes. By analyzing the effects of Irisin on these specific cell populations, our aim is to gain a comprehensive understanding of its influence throughout the entire differentiation process, rather than solely concentrating on the final differentiated cells. This approach enables us to obtain insights into the broader effects of Irisin on the cellular dynamics and mechanisms involved in adipogenesis.

This article corrects the following:

The new role of riluzole in the treatment of pancreatic cancer through the apoptosis and autophagy pathways

Rulin Sun, Xujun He, Xiaoting Jiang, Houquan Tao

J Cell Biochem 2021; 122: 934–944.

doi:10.1002/jcb.29533

First Published online: November 11, 2019

In the original version of this article, the authors selected the wrong image to depict migration inhibition of PANC1 cells treated with 200µM of riluzole, resulting in panel duplication. The correct Figure 3B is shown below.

This correction doesn't change the results and conclusions. The authors apologize for any confusion this error may have caused.

The complex impacts of prolonged morphine exposure continue to be a significant focus in the expanding area of addiction studies. This research investigates the effectiveness of a combined treatment using Cabergoline and Mdivi-1 to counteract the neuroadaptive changes caused by in vitro morphine treatment. The impact of Methadone, Cabergoline, and a combination of Cabergoline and Mdivi-1 on the cellular and molecular responses associated with Morphine-induced changes was studied in human Neuroblastoma (SK-N-MC) and Glioblastoma (U87-MG) cell lines that were exposed to prolong Morphine treatment. Cabergoline and Mdivi-1 combined treatment effectively influenced the molecular alterations associated with neuroadaptation in chronic morphine-exposed neural cells. This combination therapy normalized autophagy and reduced oxidative stress by enhancing total-antioxidant capacity, mitigating apoptosis, restoring BDNF expression, and balancing apoptotic elements. Our research outlines morphine's dual role in modulating mitochondrial dynamics via the dysregulation of the autophagy–apoptosis axis. This emphasizes the significant involvement of DRP1 activity in neurological adaptation processes, as well as disturbances in the dopaminergic pathway during in vitro chronic exposure to morphine in neural cells. This study proposes a novel approach by recommending the potential effectiveness of combining Cabergoline and Mdivi-1 to modulate the neuroadaptations caused by morphine. Additionally, we identified BDNF and PCNA in neural cells as potential neuroprotective markers for assessing the effectiveness of drugs against opioid toxicity, emphasizing the need for further validation. The study uncovers diverse effects observed in pretreated morphine glioblastoma cells under treatment with Cabergoline and methadone. This highlights the potential for new treatments in the DRD2 pathway and underscores the importance of investigating the interplay between autophagy and apoptosis to advance research in managing cancer-related pain. The study necessitates an in-depth investigation into the relationship between autophagy and apoptosis, with a specific emphasis on protein interactions and the dynamics of cell signaling.

Withdrawn: ‘LncRNA LUADT1 regulates miR-34a/SIRT1 to participate in chondrocyte apoptosis’ by Su Ni, Chao Xu, Chao Zhuang, Gongyin Zhao, Chenkai Li, Yuji Wang, Xihu Qin, J Cell Biochem (https://doi.org/10.1002/jcb.29637). The above article, published online on 7 February 2020 in Wiley Online Library (https://onlinelibrary.wiley.com/doi/10.1002/jcb.29637) has been withdrawn by agreement between the journal's Editor in Chief, Christian Behl, and Wiley Periodicals LLC.

The withdrawal has been agreed following no response from the author to requests to sign the Journal's publishing license.

Retraction: “MiR-137 functions as a tumor suppressor in pancreatic cancer by targeting MRGBP” by Feng Ding, Shuang Zhang, Shaoyang Gao, Jian Shang, Yanxia Li, Ning Cui, and Qiu Zhao, J Cell Biochem. 2018; 4799-4807: The above article, published online on 13 January 2018 in Wiley Online Library (https://doi.org/10.1002/jcb.26676) 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 after the authors stated that errors occurred during figure compilation, and that the experimental data in the article could not be verified. The investigation additionally revealed inconsistencies in several image elements. Thus, the editors consider the conclusions of this article to be invalid.

Hao Sun, Shu Hu, Ziji Zhang, Jiayong Lun, Weiming Liao, Zhiqi Zhang

In the original version of this article, the authors wrongly assembled Figure 5A resulting in the IHC staining of SOX9 for the hBMSC-320c-Exos group to be mistakenly used in both Figures 5A and 5B. The correct Figure 5A is shown below.

This correction doesn't change the results and conclusions. The authors apologize for any confusion this error may have caused.