Cell Biology International Research Articles

RETRACTION:Lack of MicroRNA-155 Ameliorates Renal Fibrosis by Targeting PDE3A/TGF-β1/Smad Signaling in Mice with Obstructive Nephropathy.

W. Xi, X. Zhao, M. Wu, W. Jia, and H. Li, "Lack of MicroRNA-155 Ameliorates Renal Fibrosis by Targeting PDE3A/TGF-β1/Smad Signaling in Mice with Obstructive Nephropathy",Cell Biology International 42, no. 11 (2018): 1523-1532. https://doi.org/10.1002/cbin.11038 The above article, published online on 6 August 2018 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Sergio Schenkman; the International Federation for Cell Biology; and John Wiley & Sons Ltd. The retraction has been agreed due to concerns raised by third parties on the data presented in the article. Several flaws and inconsistencies between results presented and experimental methods described were found. Furthermore, several image elements in Figure 2 A were found to have been published previously in a different scientific context. Thus, the editors consider the conclusions of this article to be invalid. The authors have been informed of the decision of retraction but were not available for a final confirmation.

Isolation and propagation of bovine blood-derived macrophages using a mixed culture with bovine endothelial B46 cells.

Macrophages are innate immune cells with multiple functions such as phagocytosis, cytokine production, and antigen presentation. Since macrophages play critical roles in some bacterial infectious diseases in cattle, including tuberculosis, paratuberculosis, and brucellosis, the in vitro culturing of bovine macrophages is useful for evaluating host-pathogen interactions at the cellular and molecular levels. We have previously reported the establishment of two immortalized bovine liver sinusoidal cell lines, endothelial B46 cells and myofibroblast-like A26 cells (Cell Biology International, 40, 1372-1379, 2016). In this study, we investigated the use of these cell lines as feeder cells that support the proliferation of bovine blood-derived macrophages (BBMs). Notably, the B46 cell line efficiently acts as feeder cells for the propagation of BBMs. Compared with primary cultured vascular endothelial cells, the infinite proliferation ability of B46 cells is more beneficial for preparing confluent feeder layers. In conclusion, this study provides a simple and efficient protocol for the isolation and propagation of BBMs using a primary mixed culture of bovine whole blood with B46 feeder cells. Isolated BBMs are expected to be useful for developing in vitro models for studying the interactions between bovine pathogens and host immune cells.

Withdrawn: MicroRNA-214-3p protects against myocardial ischemia-reperfusion injury by targeting demethylase lysine demethylase 3A.

The above article from Cell Biology International, published online on 5 December 2022, on Wiley Online Library (https://doi.org/10.1002/cbin.11920), has been withdrawn by agreement between the journal Editor in Chief, Sergio Schenkman, and John Wiley and Sons Ltd. The withdrawal has been agreed due to a technical error at the publisher that caused the article to be mistakenly published online.

Withdrawn: Ticagrelor reduces myocardial cell injury induced by myocardial ischemia/reperfusion in diabetic rats by activating JAK2/STAT3.

The above article from Cell Biology International, published online on 5 December 2022, on Wiley Online Library (https://doi.org/10.1002/cbin.11940), has been withdrawn by agreement between the journal Editor in Chief, Sergio Schenkman, and John Wiley and Sons Ltd. The withdrawal has been agreed due to a technical error at the publisher that caused the article to be mistakenly published online although it had been rejected due to evidence that the peer review process for this paper was manipulated.

Withdrawal.

Withdrawal: Wei Deng, Jing Wu, Wei Zheng, Dongling Li, Hongyu Kuang, RNF150 suppresses thyroid carcinoma by inactivating the p38 pathway via ubiquitination of ASK1, Cell Biology International 2022 (https://doi.org/10.1002/cbin.11786). The above article, published online on 1 March 2022 in Wiley Online Library (wileyonlinelibrary.com), has been withdrawn by agreement between the Editor-in-Chief, Sergio Schenkman, and John Wiley & Sons Ltd. The withdrawal has been agreed due to the authors not completing a copyright license agreement form.

Retraction.

Retraction: Methyltransferase-like 3 (METTL3) attenuates cardiomyocyte apoptosis with myocardial ischemia-reperfusion (I/R) injury through miR-25-3p and miR-873-5p by Xiangmei Zhao, Lei Yang, and Lijie Qin. The above article from Cell Biology International, published online on September 22, 2021, in Wiley Online Library (https://doi.org/10.1002/cbin.11706) has been retracted by agreement among the authors, the Journal's Editor-in-Chief Sergio Schenkmann, and John Wiley & Sons Ltd. on behalf of the International Federation for Cell Biology. The retraction has been agreed after the authors asked to retract and stated that the underlying data of the article were lost and could not be verified. The authors were not available for a final confirmation of the retraction.

The Potential of Medicinal Plants and Bioactive Compounds in the Fight Against COVID-19

The Potential of Medicinal Plants and Bioactive Compounds in the Fight Against COVID-19

Profesor Andrzej Grębecki (1934-2021) - badacz fizjologii ruchu komórek, nauczyciel, wychowawca

14 stycznia 2021 r. po długiej chorobie odszedł profesor Andrzej Grębecki wybitny biolog komórki, zasłużony dla nauki w Polsce i na świecie, nauczyciel i wychowawca. Profesor Andrzej Grębecki ukończył Wydział Matematyczno-Przyrodniczy Uniwersytetu Łódzkiego w 1952 r., a w 1956 r. obronił pracę doktorską pod kierunkiem prof. Jana Dembowskiego. Profesor Grębecki przez wiele lat (1973-2002) kierował Pracownią Morfodynamiki Prostych Systemów Ruchowych w Zakładzie Biologii Komórki, Instytutu Nenckiego PAN. Ponadto aktywnie uczestniczył w życiu Instytutu, w którym m.in. pełnił funkcję zastępcy dyrektora d/s naukowych (1975-1981) oraz kierownika studium doktoranckiego (1975-1979). Przez dwie kadencje w latach 1984-1989 był przewodniczącym Rady Naukowej Instytutu Nenckiego. Profesor Grębecki w latach 1984-1989 był członkiem Rady Polskiej Sieci Biologii Komórkowej i Molekularnej UNESCO, a 1993-1997 członkiem International Commission of Protozoology. Zainteresowania naukowe profesora Grębeckiego skupiały się na badaniu mechanizmów ruchu komórek. Był On autorem ponad 160 opublikowanych pozycji naukowych, obejmujących pierwsze w literaturze prace o roli wapnia w regulacji ruchu rzęskowego. Następnie swoje zainteresowania naukowe profesor Grębecki skupił na badaniach fizjologii ruchu amebowego, których wyniki publikował w bardzo prestiżowych czasopismach międzynarodowych: m.in. Journal of Cell Science, European Journal of Cell Biology, Cell Biology International Reports. Główne założenia dotyczące teorii ogólnego skurczu kortykalnego zawarł w obszernej monografii ?Membrane and cytoskeleton flow in motile cells with emphasis on the contribution of free-living Amoebae?, opublikowanej w International Review of Cytology (1994). Dowodem międzynarodowego uznania dorobku profesora Grębeckiego było jego członkostwo w pracy komitetów redakcyjnych międzynarodowych czasopism naukowych: Acta Protozool. (Warszawa), Eur.J.Protistol. (Stuttgart) i Protistology (Omsk). Za swoje osiągnięcia naukowe i organizacyjne był wielokrotnie nagradzany wyróżnieniami i odznaczeniami państwowymi (m.in. Krzyż Oficerski Orderu Odrodzenia Polski - 1998).

The Serratia grimesii outer membrane vesicles-associated grimelysin triggers bacterial invasion of eukaryotic cells.

Serratia grimesii are facultative pathogenic bacteria that can penetrate a wide range of host cells and cause infection, especially in immunocompromised patients. Previously, we have found that bacterial metalloprotease grimelysin is a potential virulence determinant of S. grimesii invasion (E. S. Bozhokina et al., (2011).Cell Biology International, 35(2), 111-118). Protease is characterized as an actin-hydrolyzing enzyme with a narrow specificity toward other cell proteins. It is not known, however, whether grimelysin is transported into eukaryotic cells. Here, we show, for the first time, that S. grimesii can generate outer membrane vesicles (OMVs) displayed specific proteolytic activity against actin, characteristic of grimelysin. The presence of grimelysin was also confirmed by the Western blot analysis of S. grimesii OMVs lysate. Furthermore, confocal microscopy analysis revealed that the S. grimesii grimelysin-containing OMVs attached to the host cell membrane. Finally, pretreatment of HeLa cells with S. grimesii OMVs before the cells were infected with bacteria increased the bacterial penetration several times. These data strongly suggest that protease grimelysin promotes S. grimesii internalization by modifying bacterial and/or host molecule(s) when it is delivered as a component of OMVs.

Retraction: Fu, W., Wang, W., Wang, H., Zhu, X., Liang, Y., Kung, H. and Zhang, J. (2014), 1,3,5‐Trihydroxy‐13,13‐dimethyl‐2H‐pyran [7,6‐b] xanthone directly targets heat shock protein 27 in hepatocellular carcinoma. Cell Biol Int, 38: 272–276. doi:10.1002/cbin.10193

The above article from Cell Biology International, published online on 07 October 2013 in Wiley Online Library (wileyonlinelibrary.com) has been retracted by agreement between the authors, the journal Editor‐in‐Chief and John Wiley & Sons Ltd. The retraction has been agreed due to an error in the detection method used.

German Society for Cell Biology International Meeting Report

German Society for Cell Biology International Meeting Report

Retracted: Knockdown of tumor protein D52-like 2 induces cell growth inhibition and apoptosis in oral squamous cell carcinoma.

The above article, published online on 13 October 2014 in Wiley Online Library (http://onlinelibrary.wiley.com/doi/10.1002/cbin.10388/abstract), has been retracted by agreement between the authors, the journal Editor, Sergio Schenkman, and John Wiley & Sons Ltd. The retraction has been agreed because the authors discovered after publication that one of the cell lines described in the article had been unintentionally misidentified. The experiments described in the article as being conducted on Human Oral Squamous Cell Carcinoma cell line KB were in fact conducted on a Human Oral Epidermal-like Cancer cell line. The authors and publisher apologise for any inconvenience. References He Y, Chen F, Cai Y and Chen S (2015) Knockdown of tumor protein D52-like 2 induces cell growth inhibition and apoptosis in oral squamous cell carcinoma. Cell Biology International 39: 264-271. doi: 10.1002/cbin.10388.

Knockdown of tumor protein D52-like 2 induces cell growth inhibition and apoptosis in oral squamous cell carcinoma.

Tumor protein D52-like 2 (TPD52L2) and its family members form homo- and hetero-meric complexes essential for cell proliferation in multiple human cancers. TPD52L2 is involved in cell migration and attachment in oral squamous cell carcinoma (OSCC). To confirm the role of TPD52L2 in OSCC, we employed the lentivirus-delivered small interfering RNA (siRNA) technique to knock down TPD52L2 expression in two OSCC cell lines, CAL27, and KB. Knockdown of TPD52L2 by RNA interference markedly suppressed cell proliferation and colony formation. Cell cycle analysis showed that depletion of TPD52L2 led to CAL27 cells arrest in the S phase. We found an excessive accumulation of cells in the sub-G1 phase, which can represent apoptotic cells. TPD52L2 silencing also induced the cleavage of PARP. These results suggest that TPD52L2 is involved in OSCC cell growth and serves as a potential therapeutic target in human OSCC.

Effects of DNA Demethylation on Human Intervertebral Disk Cells: Pilot study

Introduction The intervertebral disk (IVD) cell distribution depends on the developmental stage of the human disk.1 DNA methylation has been shown to be essential to mammalian development,2,3 and aberrant methylation patterns are a common feature of many kinds of age-related diseases.3 We hypothesize that the methylation status of the promoter region of the genomic DNA affects cell proliferation, progression, and alterations in the gene expression of IVD cells. Materials and Methods IVD tissues were obtained from donors undergoing anterior lumbar discectomy procedures with Institutional Review Board approval. The tissues were transported to the laboratory, minced and immediately underwent cell isolation by sequential enzyme digestion. The digested cells were centrifuged and seeded in culture dishes, supplemented with complete medium (DMEM/F12) containing 10% fetal bovine serum (FBS), 1% L-glutamine, and 1% antibiotic. The demethylation agent 5-azacytidine (5-aza-C)4 was used to inhibit DNA methylation in IVD cells. The cells were then plated and treated with 5-aza-C followed by cell proliferation assay by MMT assay, cell progression by fluorescent cell sorting, and analyzed for gene regulation changes by real time PCR. Results Our results demonstrate that 5-azacytidine treatment inhibits cell proliferation in both dose-dependent and time-dependent manners. Cell cycle analysis revealed that 5-azacytidine (5 µM) treatment significantly increased the percentage of cells within the sub-G1 phase, suggestive of DNA fragmentation and apoptotic cell death. 5Aza-C (5 µM) treatment also increases the percentage of cells in S phase and G2/M phase indicating cell arrest. Gene expression analysis following 5-azaC treatment revealed that the MMP-1, MMP-13, IL-1b, and IL-6 were upregulated, whereas the anabolic gene aggrecan was downregulated. Conclusion The experimentally-induced loss of DNA methylation results in the inhibition of cell proliferation and an increase in apoptotic cell death. Furthermore, demethylation results in both increased gene transcription of catabolic and inflammatory genes as well as a downregulation of aggrecan, thus confirming a cause-and-effect relationship between DNA demethylation and transcription of these genes in IVD cells. DNA demethylation has been previously shown to inhibit cell proliferation5 and induce apoptotic cell death5,6 in different cell types. Our results suggest that demethylation of IVD cells may be one of the influential causes for IVD degeneration. Further studies are required to confirm our findings and to better understand the effects of aberrant DNA methylation on IVD biology and disease pathophysiology. I confirm having declared any potential conflict of interest for all authors listed on this abstract Yes Disclosure of Interest None declared Guehring et al. European Spine Journal 2010;19(1):113–121 Takebayashi et al. Molecular and Cellular Biology 2007;27(23):8243–8258 Christensen et al. PLoS Genetics 2009;5(8) Quddus et al. Journal of Clinical Investigation 1993;92:38–53 Nilsson et al. Journal of Endocrinology 2005;186(1):241–249 Ho et al. Cell Biology International 2006;30(3):288–294

WITHDRAWN: Epigenetic control of TNAP expression in Pseudoxanthoma elasticum fibroblasts.

This paper published as an Immediate Publication on 26 January 2012 was withdrawn by the Editorial Board of Cell Biology International on 16 February 2012.

Microarray analysis of oxidized low-density lipoprotein (ox-LDL)-regulated genes in human coronary artery smooth muscle cells

Recent studies suggest that circulating LDL (low-density lipoproteins) play a central role in the pathogenesis of atherosclerosis, and the oxidized form (ox-LDL) is highly atherogenic. Deposits of ox-LDL have been found in atherosclerotic plaques, and ox-LDL has been shown to promote monocyte recruitment, foam cell formation and the transition of quiescent and contractile vascular SMCs (smooth muscle cells) to the migratory and proliferative phenotype. SMC phenotype transition and hyperplasia are the pivotal events in the pathogenesis of atherosclerosis. To comprehend the complex molecular mechanisms involved in ox-LDL-mediated SMC phenotype transition, we have compared the differential gene expression profiles of cultured quiescent human coronary artery SMCs with cells induced with ox-LDL for 3 and 21 h using Affymetrix HG-133UA cDNA microarray chips. Assignment of the regulated genes into functional groups indicated that several genes involved in metabolism, membrane transport, cell–cell interactions, signal transduction, transcription, translation, cell migration, proliferation and apoptosis were differentially expressed. Our data suggests that the interaction of ox-LDL with its cognate receptors on SMCs modulates the induction of several growth factors and cytokines, which activate a variety of intracellular signalling mechanisms (including PI3K, MAPK, Jak/STAT, sphingosine, Rho kinase pathways) that contribute to SMC transition from the quiescent and contractile phenotype to the proliferative and migratory phenotype. Our study has also identified several genes (including CDC27, cyclin A1, cyclin G2, glypican 1, MINOR, p15 and apolipoprotein) not previously implicated in ox-LDL-induced SMC phenotype transition and substantially extends the list of potential candidate genes involved in atherogenesis.

Addressing the design of in vitro models for the investigation of microcystins: The essential role of transporter‐mediated uptake

This article discusses the need for transporter-mediated uptake for investigations addressing the mechanism of action of microcystins [with reference to the previous article in Cell Biology International by de Souza Votto (2007) 31:1359-1366].

Another decade of advances in research on primary cilia, porosomes and neosis: some passing thoughts at 70

This editorial contains some of my reflections on a career spanning almost 50 years in biomedical research at the cellular level and over 12 years as Editor-in-Chief of Cell Biology International, at the time of my 70th birthday. It is gratifying that I have been involved in some of the more important organelles and processes that have come to the forefront of cell research today, and I have chosen just three examples to illustrate this point.

Cell Biology International in New Livery: Portland Press becomes our Publisher

Cell Biology International (CBI) was published originally by Academic Press (AP) for the International Federation for Cell Biology (IFCB), and latterly by Elsevier after it acquired AP. A decision was made by the IFCB Executive almost 2 years ago to move to Portland Press Limited, the not‐for‐profit wholly owned subsidiary of the Biochemical Society, based in London. However, we have had to stay with Elsevier throughout 2009 in order to fulfill a 5‐year contract.

Corrigendum to “Pre‐adipocytes commitment to neurogenesis 1: Preliminary localisation of cholinergic molecules” [Cell Biology International, 33 (2009) 594–601

DOI of original article: 10.1016/j.cellbi.2009.02.014.* Corresponding author. Tel.: þ39 0103537311; fax: þ39 0103537803.E-mail address: chiara.guida@unige.it (C. Guida).1065-6995/$ - see front matter 2009 International Federation for Cell Biology. Published by Elsevier Ltd. All rights reserved.doi:10.1016/j.cellbi.2009.06.021Cell Biology International 33 (2009) 1125www.elsevier.com/locate/cellbi