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  • Artikel  (10.795)
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  • Springer  (10.795)
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  • 1
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    Gene therapy: a double-edged sword with great powers (2020)
    Springer
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    Publikationsdatum: 2020-07-21
    Print ISSN: 0300-8177
    Digitale ISSN: 1573-4919
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    OP16 induces deadly autophagy and apoptosis of cells by inhibiting Akt in esophageal squamous cell carcinoma (2020)
    Springer
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    Publikationsdatum: 2020-07-15
    Print ISSN: 0300-8177
    Digitale ISSN: 1573-4919
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Long non-coding RNA FOXD3-AS1 regulates the expression and secretion of IL-25 in nasal epithelial cells to inhibit Th2 type immunoreaction in allergic rhinitis (2020)
    Springer
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    Publikationsdatum: 2020-07-15
    Print ISSN: 0300-8177
    Digitale ISSN: 1573-4919
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Isoprenaline induces epithelial–mesenchymal transition in gastric cancer cells (2015)
    Springer
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    Publikationsdatum: 2015-08-09
    Beschreibung: The emerging role of stress-related signaling in regulating cancer development and progression has been recognized. However, whether stress serves as a mechanism to promote gastric cancer metastasis is not clear. Here, we show that the β 2 -AR agonist, isoprenaline, upregulates expression levels of CD44 and CD44v8-10 in gastric cancer cells. CD44, a cancer stem cell-related marker, is expressed at high levels in gastric cancer tissues, which strongly correlates with the occurrence of epithelial–mesenchymal transition (EMT)-associated phenotypes both in vivo and in vitro. Combined with experimental observations in two human gastric cancer cell lines, we found that β 2 -AR signaling can initiate EMT. It led to an increased expression of mesenchymal markers, such as α-SMA, vimentin, and snail at mRNA and protein levels, and conversely a decrease in epithelial markers, E-cadherin and β-catenin. Isoprenaline stimulation of β2-AR receptors activates the downstream target STAT3, which functions as a positive regulator and mediated the phenotypic switch toward a mesenchymal cell type in gastric cancer cells. Our data provide a mechanistic understanding of the complex signaling cascades involving stress-related hormones and their effects on EMT. In light of our observations, pharmacological interventions targeting β 2 -AR-STAT3 signaling can potentially be used to ameliorate stress-associated influences on gastric cancer development and progression.
    Print ISSN: 0300-8177
    Digitale ISSN: 1573-4919
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Intracellular angiotensin (1–7) increases the inward calcium current in cardiomyocytes. On the role of PKA activation (2015)
    Springer
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    Publikationsdatum: 2015-08-14
    Beschreibung: The influence of intracellular administration of angiotensin (1–7) (Ang 1–7) on the inward calcium current was investigated in myocytes isolated from the left ventricle of Wistar Kyoto rat hearts using the patch-clamp technique. The results indicated: (1) the intracellular administration of Ang (1–7) (100 nM) enhanced the peak inward calcium current ( I Ca ); (2) the intracellular administration of A779 (100 nM) which a Mas receptor inhibitor, abolished the effect of Ang (1–7) on the calcium current; (3) the activation of PKA and consequent phosphorylation of calcium channels seems to be the mechanism involved in the increment of calcium current induced by the heptapeptide because the intracellular dialysis of the PKA inhibitor suppressed the effect of the heptapeptide; (4) the effect of Ang (1–7) was not related to its secretion into the extracellular space; (5)intracellular dialysis of Ang II (100 nM) has an opposite effect and reduced the peak I Ca ; (6) extracellular administration of Ang II (100 nM) to cells previously dialyzed with Ang (1–7) also reduced the peak I Ca previously enhanced by Ang (1–7); and (7) intracellular Ang (1–7) reduced the heart cell volume. Implications for heart contractility were discussed.
    Print ISSN: 0300-8177
    Digitale ISSN: 1573-4919
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    MD2 expression is reduced in large airways of smokers and COPD smokers (2015)
    Springer
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    Publikationsdatum: 2015-08-14
    Beschreibung: Toll-like receptor 4 (TLR4) signaling requires a number of accessory proteins to initiate a signal. MD-2 is one of the accessory proteins with a relevant role in lipopolysaccharide responses. Although cigarette smoke increases TLR4 expression, TLR4 signaling is altered in smokers and in smokers COPD patients. The main aims of this study were to explore whether MD2 is altered in large and small airways of COPD and of smokers without COPD. The expression of MD2 ex vivo was assessed by immunohistochemistry in surgical specimens from current smokers COPD (s-COPD; n  = 14), smokers without COPD (S; n  = 7), and from non-smoker non-COPD subjects (C; n  = 11. The in vitro effects of cigarette smoke extracts on the MD2 expression in a human bronchial epithelial cell line (16-HBE) were also assessed by flow cytometry. MD2 is reduced in the epithelium and in the submucosa in large airways but not in the epithelium and in the submucosa in small airways of smokers and of s-COPD. The expression of MD2 in the submucosa of the large airways is significantly higher in comparison to the submucosa of the small airways in all the studied groups. In vitro, cigarette smoke is able to increase TLR4 but it reduces MD2 in a dose-dependent manner in bronchial epithelial cells. Cigarette smoke may alter innate immune responses reducing the expression of the MD2, a molecule with an important role in TLR4 signaling.
    Print ISSN: 0300-8177
    Digitale ISSN: 1573-4919
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
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    miR-526a regulates apoptotic cell growth in human carcinoma cells (2015)
    Springer
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    Publikationsdatum: 2015-08-14
    Beschreibung: MicroRNAs (miRNAs) play vital roles in the regulation of cell cycle, cell growth, apoptosis, and tumorigenesis. Our previous studies showed that miR-526a positively regulated innate immune response by suppressing CYLD expression, however, the functional relevance of miR-526a expression and cell growth remains to be evaluated. In this study, miR-526a overexpression was found to promote cancer cell proliferation, migration, and anchor-independent colony formation. The molecular mechanism(s) of miR-526a-mediated growth stimulation is associated with rapid cell cycle progression and inhibition of cell apoptosis by targeting CYLD. Taken together, these results provide evidence to show the stimulatory role of miR-526a in tumor migration and invasion through modulation of the canonical NF-κB signaling pathway.
    Print ISSN: 0300-8177
    Digitale ISSN: 1573-4919
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
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    Effects of flavonoids on expression of genes involved in cell cycle regulation and DNA replication in human fibroblasts (2015)
    Springer
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    Publikationsdatum: 2015-08-14
    Beschreibung: Flavonoids have been studied as potential agents in medicine for many years. Among them, genistein was found to be active in various biological systems, mainly in prevention of cancer. Our recent work supported the idea that genistein also impacts multiple cellular processes in healthy fibroblasts; however, its effects on cell cycle-related pathways remained to be elucidated. Thus, in this work, high throughput screening with microarrays coupled to real-time quantitative Reverse Transcription PCR analyses was employed to study the changes in expression of key genes associated with cell cycle regulation and/or DNA replication in response to genistein, kaempferol, daidzein, and mixtures of genistein and either kaempferol or daidzein. Among them, genistein was found as the most significantly modulating, in a time- and dose-dependent manner, compound of activity of studied genes, whose products are involved in different phases of the cell cycle and/or in regulatory processes important for DNA replication and cell growth. It considerably reduced the efficiency of expression of genes coding for MCM2-7 and MCM10 helicases, as well as some other proteins involved in the S phase control. In addition, genistein caused cell cycle arrest in the G2/M phase, which was accompanied by activation of CDKN1A , CDKN1C , CDKN2A , CDKN2B , CDKN2C, and GADD45A genes, as well as down-regulation of several mRNAs specific for this stage, demonstrated by transcriptomic assessments. We believe that studies described in this paper will be helpful in elucidating molecular mechanisms of action of genistein as modulator of cell cycle and inhibitor of DNA replication in humans.
    Print ISSN: 0300-8177
    Digitale ISSN: 1573-4919
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Rosiglitazone suppresses HIV-1 Tat-induced vascular inflammation via Akt signaling (2015)
    Springer
    Details
    Publikationsdatum: 2015-08-14
    Beschreibung: Peroxisome proliferator-activated receptor gamma (PPARƔ) contributes to human immunodeficiency virus (HIV)-1-induced dysfunction of brain endothelial cells. The aim of the present study was to evaluate the protection mechanism of PPARƔ against Tat-induced responses of adhesion molecules. We measured the protein expressions of intercellular adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 in human brain microvascular endothelial cells (hCMEC/D3) and C57BL/6J mouse brain microvessels with Western blotting and immunofluorescent labeling. The mRNA levels of ICAM-1 and VCAM-1 were determined by real-time reverse-transcriptase polymerase chain reaction. HIV-1 Tat induced overexpression of ICAM-1 but not VCAM-1 in both hCMEC/D3 and brain microvessels, this response was attenuated by treatment with the PPARƔ agonist rosiglitazone. Tat-mediated upregulation of ICAM-1 and VCAM-1 levels were abolished by the addition of PPARƔ antagonist GW9662 and the Akt inhibitor KP3721, indicating that Akt signaling is involved in the PPARƔ-mediated protection of Tat-induced adhesion molecule upregulation. These results show that Akt signaling plays a key role in PPARƔ’s vascular inflammatory effects that contribute to blood–brain barrier damage.
    Print ISSN: 0300-8177
    Digitale ISSN: 1573-4919
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
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    Apigenin promotes osteogenic differentiation of human mesenchymal stem cells through JNK and p38 MAPK pathways (2015)
    Springer
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    Publikationsdatum: 2015-08-14
    Beschreibung: Apigenin is a plant-derived flavonoid and has been reported to prevent bone loss in ovariectomized mice, but the role of apigenin on osteogenic differentiation of human mesenchymal stem cells (hMSCs) has not been reported. In the present study, the effect of apigenin on osteogenic differentiation of hMSCs was explored. Our results showed that apigenin treatment significantly increased alkaline phosphatase (ALP) activity and mineralization in hMSCs. RT-PCR revealed that apigenin markedly up-regulated the mRNA expression of osteopontin (OPN) and the transcription factors runt-related transcription factor 2 (Runx2). The expression of Runx2 and osterix (OSX) proteins were also increased in hMSCs differentiating into osteoblasts after treatment with apigenin. Furthermore, we investigated the signaling pathways responsible for osteogenic differentiation of apigenin in hMSCs. We found that apigenin treatment significantly increased the levels of p-JNK, p-p38 in hMSCs and addition of the inhibitors of JNK (SP600125) or p38 MAPK (SB203580) eliminated the stimulating effects of apigenin. In addition, addition of SP600125 or SB203580 also blocked apigenin-induced ALP activity, OPN, Runx2, and OSX expression and meanwhile inhibited bone nodule formation. Taken together, these findings suggest apigenin promotes the osteogenesis of hMSCs through activation of JNK and p38 MAPK signal pathways which leads to Runx2 and OSX expressions to induce the formation of bone nodule.
    Print ISSN: 0300-8177
    Digitale ISSN: 1573-4919
    Thema: Biologie , Chemie und Pharmazie , Medizin
    Publiziert von Springer
    Standort Signatur Erwartet Verfügbarkeit
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