Journal of Cellular Physiology最新文献

RETRACTION: H. Zhao, G.-H. Zheng, G.-C. Li, L. Xin, Y.-S. Wang, Y. Chen, and X.-M. Zheng, “Long Noncoding RNA LINC00958 Regulates Cell Sensitivity to Radiotherapy Through RRM2 by Binding to microRNA-5095 in Cervical Cancer,” Journal of Cellular Physiology 234, no. 12 (2019): 23349-23359. https://doi.org/10.1002/jcp.28902.

The above article, published online on 06 June 2019 in Wiley Online Library (wileyonlinelibrary.com), and has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC.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 same tumor image was detected between Figure 6 A in this article and Figure 7B in another article (Guo, et al. 2019 [https://doi.org/10.18632/aging.102271]. The third party reported additional image duplications between Figure 2B in this article and other articles by different authors (Guo, et al. 2018 [https://doi.org/10.1186/s12964-018-0290-6]; (Liu, et al. 2019 [https://doi.org/10.1002/jcp.27893]; (Wen, et al. 2019 [https://doi.org/10.1096/fj.201900310 R]; and (Ou, et al. 2020 [https://doi.org/10.1016/j.ebiom.2020.102694]. Each mentioned article describes a different scientific context. The authors did not respond to an inquiry by the publisher. The retraction has been agreed on because the evidence of image duplication with other articles fundamentally compromises the conclusions reported in this article. The authors did not respond to our notice regarding the retraction.

RETRACTION: J. Li, S. Zhang, Y. Zou, L. Wu, M. Pei, and Y. Jiang, “MiR-145 Promotes MiR-133b Expression Through c-myc and DNMT3A-mediated Methylation in Ovarian Cancer Cells,” Journal of Cellular Physiology 235, no. 5 (2020): 4291-4301, https://doi.org/10.1002/jcp.29306.

The above article, published online on 14 October 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Roberth Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Specifically, instances of duplicated image elements were identified in Figures 2 d, 3 d, and 5 g. Therefore, the article is retracted as the editors consider its conclusions to be invalid. The authors have been informed of the decision of retraction.

RETRACTION: D.-C. Liu, L.-L. Song, Q. Liang, L. Hao, Z.-G. Zhang, and C.-H. Han, “Long Noncoding RNA LEF1-AS1 Silencing Suppresses the Initiation and Development of Prostate Cancer by Acting as a Molecular Sponge of miR-330-5p via LEF1 Repression,” Journal of Cellular Physiology 234, no. 8 (2019): 12727-12744. https://doi.org/10.1002/jcp.27893.

The above article, published online on 05 January 2019 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 images shared overlapping sections in Figure 3B in this article, and this duplication was confirmed by the publisher. The third party also reported that duplicated images in this article had been detected in subsequent articles by different authors, each of which describes different experimental conditions (Zhao, et al. 2019 [https://doi.org/10.1002/jcp.28902]); (Ou, et al. 2020 [https://doi.org/10.1016/j.ebiom.2020.102694]; and (Sha, et al. 2021 [https://doi.org/10.18632/aging.203088]). The authors did not respond to an inquiry by the publisher. The retraction has been agreed on because the evidence of image duplication within this article, as well as subsequent unexplained duplications with other articles, fundamentally compromises the conclusions reported in this article. The authors responded to our notice regarding the retraction but did not state their agreement nor their disagreement with the retraction.

Programmed cell death (apoptosis) is essential part of the process of tissue regeneration that also plays role in the mechanism of pathology. The phenomenon of fast and transient permeability of mitochondrial membranes by various triggers, known as permeability transition pore (mPTP) leads to the release of proapoptotic proteins and acts as an initial step in initiation of apoptosis. However, a role for mPTP was also suggested for physiology and it is unclear if there is a threshold in number of mitochondria with mPTP which induces cell death and how this mechanism is regulated in different tissues. Using simultaneous measurements of mitochondrial membrane potential and a fluorescent marker for caspase-3 activation we studied the number of mitochondria with calcium-induced mPTP opening necessary for induction of apoptosis in rat primary cortical neurons, astrocytes, fibroblasts, and cancer (BT-474) cells. The induction of apoptosis was correlated with 80%–90% mitochondrial signal loss in neural cells but only 35% in fibroblasts, and in BT-474 cancer cells over 90% of mitochondria opens mPTP before apoptosis becomes obvious. The number of mitochondria with mPTP which induce cell death did not correlate with total expression levels of proapoptotic proteins but was consistent with the Bax/Bcl-2 ratio in these cells. Calcium-induced mPTP opening increased levels of necrosis which was higher in fibroblasts compared to neurons, astrocytes and BT-474 cells. Thus, different tissues require specific numbers of mitochondria with PTP opening to induce apoptosis and it correlates to the proapoptotic/antiapoptotic proteins expression ratio in them.

The proliferation of CAR-T cells was hindered and cannot play its killing function well in solid tumors. And yet the regulatory mechanism of CAR-T cell proliferation is not fully understood. Here, we showed that recombinant expression of CD19CAR in T cells significantly increased the basal activation level of CAR-T cells and LCK activation. Both LCK and SMAD4 were essential for CAR-T cells proliferation since over-express LCK or SMAD4 significantly promotes CAR-T cells proliferation, while knock-down LCK or SMAD4 expression inhibited the proliferation of CAR-T cells seriously. More cells go into apoptosis when knock-down LCK or SMAD4 expression, and the cell cycle was arrested in G2/M or S phase, respectively. Over-express LCK or SMAD4 significantly promotes phosphorylation of PI3K and Akt, while it was inhibited when cells were treated with PI3K and Akt inhibitors (LY294002 or MK2206). Further mechanism exploration experiments showed that SMAD4 bound on the promoter region of LCK regulating its expression. Taken together, we reported that the transcription factor SMAD4 regulated the expression of LCK and further involved in the PI3K/Akt signaling pathway to affect the proliferation of CAR-T cells.

Vascular regeneration plays a vital role in tissue repair yet is drastically impaired in those with a spinal cord injury (SCI). Pericytes are of great significance as they are entwined with vessel-specific endothelial cells and actively contribute to maintaining the spinal cord's vascular network. Within the neurovascular unit (NVU), subtypes of pericytes characterized by various markers such as PDGFR-β, Desmin, CD146, and NG-2 are involved in vascular regeneration in SCI repair. Various pericyte signaling, pericyte-derived exosomes, and endothelial–pericyte interplay were revealed to participate in SCI repair or fibrotic scars. Through further understanding pericyte biology, it is aimed to accurately generate subtypes of pericytes and develop their therapeutic potential. This review focuses on recent advanced research and development of pericytes as a potential treatment for SCI.