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      EGCG Regulates Cell Apoptosis of Human Umbilical Vein Endothelial Cells Grown on 316L Stainless Steel for Stent Implantation

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          Nowadays, medical grade 316L stainless steel (316L SS) is being widely used for intravascular stents, and the drug-eluting stent (DES) system is able to significantly reduce the occurrences of in-stent restenosis. But the drugs and the polymer coating used in DES potentially induce the forming of late stent thrombosis. In order to reduce the occurrence of ISR after stent implantation, the development of novel drugs for DESs is urgently needed.


          This study aimed to investigate the potential mechanisms of epigallocatechin-3-gallate (EGCG) on human umbilical vein endothelial cells (HUVEC) grown on 316L stainless steel (316L SS) using flow cytometry and Q-PCR methods.


          Our results showed that EGCG (12.5, 25, 50, 100 μmol/L) significantly inhibited HUVEC proliferation. Flow cytometry analysis indicated that EGCG (25, 50, 100 μmol/L) induced apoptosis. Moreover, qRT-PCRrevealed that genes associated with cell apoptosis (caspase-3, 8, 9, Fas) and autophagy (Atg 5, Atg 7, Atg 12) were up-regulated after EGCG treatment.


          These findings indicate that EGCG possesses chemo preventive potential in stent coating which may serve as a novel new drug for stent implantation.

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          Most cited references 29

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          Life and death partners: apoptosis, autophagy and the cross-talk between them.

          It is not surprising that the demise of a cell is a complex well-controlled process. Apoptosis, the first genetically programmed death process identified, has been extensively studied and its contribution to the pathogenesis of disease well documented. Yet, apoptosis does not function alone to determine a cell's fate. More recently, autophagy, a process in which de novo-formed membrane-enclosed vesicles engulf and consume cellular components, has been shown to engage in a complex interplay with apoptosis. In some cellular settings, it can serve as a cell survival pathway, suppressing apoptosis, and in others, it can lead to death itself, either in collaboration with apoptosis or as a back-up mechanism when the former is defective. The molecular regulators of both pathways are inter-connected; numerous death stimuli are capable of activating either pathway, and both pathways share several genes that are critical for their respective execution. The cross-talk between apoptosis and autophagy is therefore quite complex, and sometimes contradictory, but surely critical to the overall fate of the cell. Furthermore, the cross-talk is a key factor in the outcome of death-related pathologies such as cancer, its development and treatment.
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            The regulation of autophagy - unanswered questions.

            Autophagy is an intracellular lysosomal (vacuolar) degradation process that is characterized by the formation of double-membrane vesicles, known as autophagosomes, which sequester cytoplasm. As autophagy is involved in cell growth, survival, development and death, the levels of autophagy must be properly regulated, as indicated by the fact that dysregulated autophagy has been linked to many human pathophysiologies, such as cancer, myopathies, neurodegeneration, heart and liver diseases, and gastrointestinal disorders. Substantial progress has recently been made in understanding the molecular mechanisms of the autophagy machinery, and in the regulation of autophagy. However, many unanswered questions remain, such as how the Atg1 complex is activated and the function of PtdIns3K is regulated, how the ubiquitin-like conjugation systems participate in autophagy and the mechanisms of phagophore expansion and autophagosome formation, how the network of TOR signaling pathways regulating autophagy are controlled, and what the underlying mechanisms are for the pro-cell survival and the pro-cell death effects of autophagy. As several recent reviews have comprehensively summarized the recent progress in the regulation of autophagy, we focus in this Commentary on the main unresolved questions in this field.
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              Is Open Access

              The complexity of NF-κB signaling in inflammation and cancer

              The NF-κB family of transcription factors has an essential role in inflammation and innate immunity. Furthermore, NF-κB is increasingly recognized as a crucial player in many steps of cancer initiation and progression. During these latter processes NF-κB cooperates with multiple other signaling molecules and pathways. Prominent nodes of crosstalk are mediated by other transcription factors such as STAT3 and p53 or the ETS related gene ERG. These transcription factors either directly interact with NF-κB subunits or affect NF-κB target genes. Crosstalk can also occur through different kinases, such as GSK3-β, p38, or PI3K, which modulate NF-κB transcriptional activity or affect upstream signaling pathways. Other classes of molecules that act as nodes of crosstalk are reactive oxygen species and miRNAs. In this review, we provide an overview of the most relevant modes of crosstalk and cooperativity between NF-κB and other signaling molecules during inflammation and cancer.

                Author and article information

                Drug Des Devel Ther
                Drug Des Devel Ther
                Drug Design, Development and Therapy
                11 February 2021
                : 15
                : 493-499
                [1 ]Department of Cardiology, The Second Hospital of Jilin University , Changchun, 130041, People’s Republic of China
                [2 ]Department of Nutrition and Food Hygiene, School of Public Health, Jilin University , Changchun, 130021, People’s Republic of China
                [3 ]Department of Physiology, College of Basic Medical Sciences, Jilin University , Changchun, 130021, People’s Republic of China
                [4 ]Jilin Engineering Research Center of Public Health Detection , Changchun, 130021, People’s Republic of China
                Author notes
                Correspondence: Kun Xu Department of Nutrition and Food Hygiene, School of Public Health, Jilin University , Changchun, 130021, People’s Republic of China Email xukun@jlu.edu.cn
                © 2021 Wang et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 3, Tables: 1, References: 29, Pages: 7
                Original Research

                Pharmacology & Pharmaceutical medicine

                apoptosis, egcg, huvecs, 316 stainless steel


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