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  1. Article ; Online: Genetic deletion or tyrosine phosphatase inhibition of PTPRZ1 activates c-Met to up-regulate angiogenesis and lung adenocarcinoma growth.

    Kastana, Pinelopi / Ntenekou, Despoina / Mourkogianni, Eleni / Enake, Michaela-Karina / Xanthopoulos, Athanasios / Choleva, Effrosyni / Marazioti, Antonia / Nikou, Sophia / Akwii, Racheal G / Papadaki, Eleni / Gramage, Esther / Herradón, Gonzalo / Stathopoulos, Georgios T / Mikelis, Constantinos M / Papadimitriou, Evangelia

    International journal of cancer

    2023  Volume 153, Issue 5, Page(s) 1051–1066

    Abstract: Protein tyrosine phosphatase receptor zeta 1 (PTPRZ1) is a transmembrane tyrosine phosphatase (TP) expressed in endothelial cells and required for stimulation of cell migration by vascular endothelial growth factor ... ...

    Abstract Protein tyrosine phosphatase receptor zeta 1 (PTPRZ1) is a transmembrane tyrosine phosphatase (TP) expressed in endothelial cells and required for stimulation of cell migration by vascular endothelial growth factor A
    MeSH term(s) Animals ; Mice ; Adenocarcinoma of Lung/drug therapy ; Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/metabolism ; Endothelial Cells/metabolism ; Protein Tyrosine Phosphatases/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Tyrosine/metabolism ; Vascular Endothelial Growth Factor A/genetics ; Vascular Endothelial Growth Factor A/metabolism ; Receptor-Like Protein Tyrosine Phosphatases, Class 5/metabolism ; Proto-Oncogene Proteins c-met/metabolism
    Chemical Substances Protein Tyrosine Phosphatases (EC 3.1.3.48) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Tyrosine (42HK56048U) ; Vascular Endothelial Growth Factor A ; Ptprz1 protein, mouse (EC 3.1.3.48) ; Receptor-Like Protein Tyrosine Phosphatases, Class 5 (EC 3.1.3.48) ; Proto-Oncogene Proteins c-met (EC 2.7.10.1)
    Language English
    Publishing date 2023-06-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.34564
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 478: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 576: Show issues

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  2. Article: Insight into the role of chondroitin sulfate E in angiogenesis

    Kastana, Pinelopi / Choleva, Effrosyni / Karamanos, Nikos / Papadimitriou, Evangelia / Poimenidi, Evangelia / Sugahara, Kazuyuki

    FEBS journal. 2019 Aug., v. 286, no. 15

    2019  

    Abstract: Chondroitin sulfate E (CS‐E) is a glycosaminoglycan containing type‐E disaccharide units (sulfated at C‐4 and C‐6 of N‐acetylgalactosamine). CS‐E is covalently linked to a core protein to form chondroitin sulfate proteoglycans (PGs) that are secreted or ... ...

    Abstract Chondroitin sulfate E (CS‐E) is a glycosaminoglycan containing type‐E disaccharide units (sulfated at C‐4 and C‐6 of N‐acetylgalactosamine). CS‐E is covalently linked to a core protein to form chondroitin sulfate proteoglycans (PGs) that are secreted or associated with the plasma membrane of several types of cells. CS‐E‐containing PGs selectively interact with growth factors and chemokines and control various cellular and/or tissue processes. Angiogenesis is a process that is highly regulated in physiological conditions but deregulated in pathologies, leading to excess or deficient blood vessel formation. Angiogenesis regulation is orchestrated by numerous growth factors, such as vascular endothelial growth factor A, fibroblast growth factors and pleiotrophin, whose functions can be affected by CS‐containing PGs. In the present review, we focus on the emerging area of CS‐mediated angiogenesis and particularly on the critical assessment of data related to a potential role of CS‐E in controlling endothelial cell functions, focusing on angiogenesis regulation and vascular homeostasis in health and disease.
    Keywords angiogenesis ; blood vessels ; chemical bonding ; chemokines ; chondroitin sulfate ; endothelial cells ; fibroblast growth factors ; homeostasis ; plasma membrane ; proteoglycans ; vascular endothelial growth factor A
    Language English
    Dates of publication 2019-08
    Size p. 2921-2936.
    Publishing place John Wiley & Sons, Ltd
    Document type Article
    Note REVIEW
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.14830
    Database NAL-Catalogue (AGRICOLA)

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    In stock of ZB MED Bonn / Germany

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  3. Article ; Online: Insight into the role of chondroitin sulfate E in angiogenesis.

    Kastana, Pinelopi / Choleva, Effrosyni / Poimenidi, Evangelia / Karamanos, Nikos / Sugahara, Kazuyuki / Papadimitriou, Evangelia

    The FEBS journal

    2019  Volume 286, Issue 15, Page(s) 2921–2936

    Abstract: Chondroitin sulfate E (CS-E) is a glycosaminoglycan containing type-E disaccharide units (sulfated at C-4 and C-6 of N-acetylgalactosamine). CS-E is covalently linked to a core protein to form chondroitin sulfate proteoglycans (PGs) that are secreted or ... ...

    Abstract Chondroitin sulfate E (CS-E) is a glycosaminoglycan containing type-E disaccharide units (sulfated at C-4 and C-6 of N-acetylgalactosamine). CS-E is covalently linked to a core protein to form chondroitin sulfate proteoglycans (PGs) that are secreted or associated with the plasma membrane of several types of cells. CS-E-containing PGs selectively interact with growth factors and chemokines and control various cellular and/or tissue processes. Angiogenesis is a process that is highly regulated in physiological conditions but deregulated in pathologies, leading to excess or deficient blood vessel formation. Angiogenesis regulation is orchestrated by numerous growth factors, such as vascular endothelial growth factor A, fibroblast growth factors and pleiotrophin, whose functions can be affected by CS-containing PGs. In the present review, we focus on the emerging area of CS-mediated angiogenesis and particularly on the critical assessment of data related to a potential role of CS-E in controlling endothelial cell functions, focusing on angiogenesis regulation and vascular homeostasis in health and disease.
    MeSH term(s) Animals ; Blood Vessels/metabolism ; Blood Vessels/physiology ; Chemokines/metabolism ; Chondroitin Sulfates/metabolism ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Neovascularization, Physiologic
    Chemical Substances Chemokines ; Intercellular Signaling Peptides and Proteins ; Chondroitin Sulfates (9007-28-7)
    Language English
    Publishing date 2019-04-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2173655-8
    ISSN 1742-4658 ; 1742-464X
    ISSN (online) 1742-4658
    ISSN 1742-464X
    DOI 10.1111/febs.14830
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 260: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  4. Article ; Online: The Coadministration of Levosimendan and Exenatide Offers a Significant Cardioprotective Effect to Isolated Rat Hearts against Ischemia/Reperfusion Injury.

    Leivaditis, Vasileios / Koletsis, Efstratios / Tsopanoglou, Nikolaos / Charokopos, Nikolaos / D'Alessandro, Cristian / Grapatsas, Konstantinos / Apostolakis, Efstratios / Choleva, Effrosyni / Plota, Maria / Emmanuil, Andreas / Dahm, Manfred / Dougenis, Dimitrios

    Journal of cardiovascular development and disease

    2022  Volume 9, Issue 8

    Abstract: 1) Background: The present study aims to investigate the effect of administration of Levosimendan and Exenatide in various concentrations, as well as of the coadministration of those agents in an ischemia-reperfusion injury isolated heart model. (2) ... ...

    Abstract (1) Background: The present study aims to investigate the effect of administration of Levosimendan and Exenatide in various concentrations, as well as of the coadministration of those agents in an ischemia-reperfusion injury isolated heart model. (2) Methods: After 30 min of perfusion, the hearts underwent a 30 min period of regional ischemia followed by a 120 min period of reperfusion. All animals were randomly divided into 12 experimental groups of nine animals in each group: (1) Control, (2) Sham, (3) Digox (Negative control, Digoxin 1.67 μg/min), (4) Levo 1 (Levosimendan 0.01 μg/min), (5) Levo 2 (Levosimendan 0.03 μg/mL), (6) Levo 3 (Levosimendan 0.1 μg/min), (7) Levo 4 (Levosimendan 0.3 μg/min), (8) Levo 5 (Levosimendan 1 μg/min), (9) Exen 1 (Exenatide 0.001 μg/min), (10) Exen 2 (Exenatide 0.01 μg/min), (11) Exen 3 (Exenatide 0.1 μg/min) and (12) Combi (Levosimendan 0.1 µg/mL + Exenatide 0.001 μg/min). The hemodynamic parameters were recorded throughout the experiment. Arrhythmias and coronary flow were also evaluated. After every experiment the heart was suitably prepared and infarct size was measured. Markers of myocardial injury were also measured. Finally, oxidative stress was evaluated measuring reactive oxygen species. (3) Results: A dose-dependent improvement of the haemodynamic response was observed after the administration of both Levosimendan and Exenatide. The coadministration of both agents presented an even greater effect, improving the haemodynamic parameters further than the two agents separately. Levosimendan offered an increase of the coronary flow and both agents offered a reduction of arrhythmias. A dose-dependent reduction of the size of myocardial infarction and myocardial injury was observed after administration of Levosimendan and Exenatide. The coadministration of both agents offered a further improving the above parameters. Levosimendan also offered a significant reduction of oxidative stress. (4) Conclusions: The administration of Levosimendan and Exenatide offers a significant benefit by improving the haemodynamic response, increasing the coronary flow and reducing the occurrence of arrhythmias, the size of myocardial injury and myocardial oxidative stress in isolated rat hearts.
    Language English
    Publishing date 2022-08-12
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2777082-5
    ISSN 2308-3425 ; 2308-3425
    ISSN (online) 2308-3425
    ISSN 2308-3425
    DOI 10.3390/jcdd9080263
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Pleiotrophin selectively binds to vascular endothelial growth factor receptor 2 and inhibits or stimulates cell migration depending on α

    Lamprou, Margarita / Kastana, Pinelopi / Kofina, Fani / Tzoupis, Ηaralampos / Barmpoutsi, Spyridoula / Sajib, Md Sanaullah / Koutsioumpa, Marina / Poimenidi, Evangelia / Zompra, Aikaterini A / Tassopoulos, Dimitrios / Choleva, Effrosyni / Tselios, Theodore / Mikelis, Constantinos M / Papadimitriou, Evangelia

    Angiogenesis

    2020  Volume 23, Issue 4, Page(s) 621–636

    Abstract: Pleiotrophin (PTN) has a moderate stimulatory effect on endothelial cell migration through ... ...

    Abstract Pleiotrophin (PTN) has a moderate stimulatory effect on endothelial cell migration through α
    MeSH term(s) Animals ; Carrier Proteins/chemistry ; Carrier Proteins/metabolism ; Cell Line, Tumor ; Cell Movement ; Cytokines/chemistry ; Cytokines/metabolism ; Human Umbilical Vein Endothelial Cells/metabolism ; Humans ; Integrin alphaVbeta3/metabolism ; Mice ; Models, Biological ; Molecular Dynamics Simulation ; Neovascularization, Physiologic ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein Binding ; Protein Domains ; Rats ; Signal Transduction ; Vascular Endothelial Growth Factor A/metabolism ; Vascular Endothelial Growth Factor Receptor-2/metabolism
    Chemical Substances Carrier Proteins ; Cytokines ; Integrin alphaVbeta3 ; Vascular Endothelial Growth Factor A ; pleiotrophin (134034-50-7) ; Phosphotyrosine (21820-51-9) ; Vascular Endothelial Growth Factor Receptor-2 (EC 2.7.10.1)
    Language English
    Publishing date 2020-07-17
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1484717-6
    ISSN 1573-7209 ; 0969-6970
    ISSN (online) 1573-7209
    ISSN 0969-6970
    DOI 10.1007/s10456-020-09733-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5094: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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