Journal of Cellular Physiology最新文献

Proliferative vitreoretinopathy (PVR) is a complex disease that significantly contributes to recurrent retinal detachment. Its development is notably affected by epithelial-mesenchymal transition (EMT), where apoptosis plays a crucial role as a regulator of EMT. However, the function of MeCP2 in governing apoptosis and EMT in retinal pigment epithelial (RPE) cells and its implications for PVR development have remained inadequately understood. Thus, we investigated the impact of MeCP2 on proliferation, migration, apoptosis and EMT in ARPE-19 cells to provide a fresh perspective on the etiology of PVR. The morphological changes in ARPE-19 cells induced by recombinant human MeCP2 protein and MeCP2 knockdown were observed. Wound healing assay were performed to verify the effects of recombinant human MeCP2 protein and MeCP2 knockdown on ARPE-19 cell migration. Furthermore, cell proliferation was assessed using the CCK-8 assay and flow cytometry. Western blot analysis, quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR), and immunofluorescence analysis were conducted to measure the protein levels associated with apoptosis, cell cycle and EMT. Western blot analysis and immunofluorescence assays confirmed that MeCP2 promoted EMT formation in ARPE-19 cells. The CCK-8 assay revealed that MeCP2 treatment enhanced the proliferation of ARPE-19 cells, whereas MeCP2 knockdown inhibited ARPE-19 cell proliferation. Treatment with recombinant human MeCP2 protein and MeCP2 knockdown altered the morphology of ARPE-19 cells. Wound healing assay demonstrated that MeCP2 knockdown inhibited ARPE-19 cell migration, and MeCP2 treatment promoted ARPE-19 cell migration. MeCP2 knockdown induced a G0/G1 phase block, inhibiting cell growth, and qRT-PCR data indicated reduced expression of cell cycle-related genes. Increased apoptosis was observed after MeCP2 knockdown in ARPE-19 cells. Overall, MeCP2 treatment stimulates cell proliferation, migration and EMT formation; conversely, MeCP2 knockdown inhibits EMT, cell proliferation, migration and cell cycle G1/S phase transition, and induces apoptosis.

Retraction: D. Zhao, Y. Ma, X. Li, and X. Lu, "MicroRNA-211 Promotes Invasion and Migration of Colorectal Cancer Cells by Targeting FABP4 via PPARγ," Journal of Cellular Physiology 234, no. 9 (2019): 15429-15437, https://doi.org/10.1002/jcp.28190. The above article, published online on 26 February 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Alexander Hutchison; and Wiley Periodicals LLC. The retraction has been agreed due to several instances of overlaps within and between images in Figures 2b, 2c, 5a and 5b, which should represent different experimental conditions. The authors were invited to comment on the concerns raised but did not respond. The editors consider the results and conclusion reported in this article unreliable.

Retraction: M. Soheili and M. Salami, "Lavandula Angustifolia Biological Characteristics: An in Vitro Study," Journal of Cellular Physiology 234, no. 9 (2019): 16424-16430, https://doi.org/10.1002/jcp.28311. The above article, published online on 19 February 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Alexander Hutchison; and Wiley Periodicals LLC. Following publication, concerns were raised by a third party regarding suspected overlap of the images presented in figures 6a and 6b. The authors were invited to comment on the concerns raised but did not respond. The editors consider the results and conclusion reported in this article unreliable.

Retraction: N. Gabellini, V. Masola, S. Quartesan, B. Oselladore, C. Nobile, R. Michelucci, M. Curtarello, C. Parolin, and G. Palù, Journal of Cellular Physiology 207, no. 3 (2006): 711-721. https://doi.org/10.1002/jcp.20627. The above article, published online on 03 March 2006, in Wiley Online Library (wileyonlinelibrary.com), and has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. A third party reported that the GAPDH blots in Figure 1 and Figure 6 showed evidence of image manipulation. An investigation by the publisher found evidence of duplication, resizing, and splicing between Figures 1B and 6B as well as evidence of splicing in Figures 1A and 6A. The authors did not respond to an inquiry by the publisher and a request for original data. The retraction has been agreed to because the results presented in the article can no longer be considered reliable.

Dysregulation of alternative pre-mRNA splicing plays a critical role in the progression of cancers, yet the underlying molecular mechanisms remain largely unknown. It is reported that metastasis-associated in colon cancer 1 (MACC1) is a novel prognostic and predictive marker in many types of cancers, including lung adenocarcinoma. Here, we reveal that the oncogene MACC1 specifically drives the progression of lung adenocarcinoma through its control over cancer-related splicing events. MACC1 depletion inhibits lung adenocarcinoma progression through triggering IRAK1 from its long isoform, IRAK1-L, to the shorter isoform, IRAK1-S. Mechanistically, MACC1 interacts with splicing factor HNRNPH1 to prevent the production of the short isoform of IRAK1 mRNA. Specifically, the interaction between MACC1 and HNRNPH1 relies on the involvement of MACC1's SH3 domain and HNRNPH1's GYR domain. Further, HNRNPH1 can interact with the pre-mRNA segment (comprising exon 11) of IRAK1, thereby bridging MACC1's regulation of IRAK1 splicing. Our research not only sheds light on the abnormal splicing regulation in cancer but also uncovers a hitherto unknown function of MACC1 in tumor progression, thereby presenting a novel potential therapeutic target for clinical treatment.

AMP-activated protein kinase (AMPK), a crucial regulatory kinase, monitors energy levels, conserving ATP and boosting synthesis in low-nutrition, low-energy states. Its sensitivity links microenvironmental changes to cellular responses. As the primary support structure and endocrine organ, the maintenance, and repair of bones are closely associated with the microenvironment. While a series of studies have explored the effects of specific microenvironments on bone, there is lack of angles to comprehensively evaluate the interactions between microenvironment and bone cells, especially for bone marrow mesenchymal stem cells (BMMSCs) which mediate the differentiation of osteogenic lineage. It is noteworthy that accumulating evidence has indicated that AMPK may serve as a hub between BMMSCs and microenvironment factors, thus providing a new perspective for us to understand the biology and pathophysiology of stem cells and bone. In this review, we emphasize AMPK's pivotal role in bone microenvironment modulation via ATP, inflammation, reactive oxygen species (ROS), calcium, and glucose, particularly in BMMSCs. We further explore the use of AMPK-activating drugs in the context of osteoarthritis and osteoporosis. Moreover, building upon the foundation of AMPK, we elucidate a viewpoint that facilitates a comprehensive understanding of the dynamic relationship between the microenvironment and bone homeostasis, offering valuable insights for prospective investigations into stem cell biology and the treatment of bone diseases.

Insulin resistance (IR), a hallmark of type 2 diabetes mellitus, develops in a significant number of patients with type 1 diabetes mellitus (T1DM) despite the use of insulin therapy to control glycemia. However, little is currently understood regarding the underlying mechanisms of IR in T1DM, especially within the context of chronic insulin treatment. Recent evidence suggests an important influence of glucolipotoxicity in skeletal muscle on insulin sensitivity in T1DM. Thus, this review summarizes our current knowledge regarding impairments in skeletal muscle lipid, glucose, and oxidative metabolism in the development of IR in insulin-treated T1DM.

Retraction: J. Song, C. Lu, W. Zhao, X. Shao, "Melatonin attenuates TNF-α-mediated hepatocytes damage via inhibiting mitochondrial stress and activating the Akt-Sirt3 signaling pathway," Journal of Cellular Physiology 234, no. 11 (2019): 20969-20979, https://doi.org/10.1002/jcp.28701. The above article, published online on 25 April 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the authors; the journal's Editor in Chief, Alexander Hutchison; and Wiley Periodicals LLC. The retraction has been agreed due to concerns related to the data presented in the article. Several flaws and inconsistencies between results presented and experimental methods described were found. Additionally, several image elements of the experimental data were published elsewhere in a different scientific context. The authors stated that the data has been partially generated by a third-party company. Accordingly, the conclusions of this article are considered invalid.