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<general>
<title>
<string language="el">Interference of Advanced Glycation End-products signaling with collagen cross-linking in human endothelium</string>
</title>
<language>eng</language>
<identifier>
<catalog>URI</catalog>
<entry>http://hdl.handle.net/10795/3400</entry>
</identifier>
<subject>
<string language="el">ιατρική</string>
<string language="el">βιοχημεία</string>
<string language="el">κυτταρολογία</string>
</subject>
<description>
<string language="el">Maintenance of extracellular matrix (ECM) stability is critical for vascular remodeling associated with cardiovascular diseases. Covalent cross-linking of collagen and elastin initiated by the copper-dependent lysyl oxidase (LOX) is a central event assuring ECM stability and vascular homeostasis. LOX downregulation leads to endothelial dysfunction characteristic of early atherosclerotic stages, whereas its upregulation in vascular cells can induce neointimal thickening in atherosclerosis and restenosis. Advanced Glycation End-products (AGEs), the highly reactive products of non-enzymatic glycation of proteins, lipids and nucleic acids, contribute to endothelial dysfunction, atherosclerosis and vascular injury under both normal and diabetic conditions.
The aim of the present study was to investigate the effect of AGEs in regulation of LOX gene/protein expression in human endothelial cells and to explore the potential functional impact of this interaction  in an animal model.</string>
</description>
<description>
<string language="el">1 pp.</string>
</description>
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<lifecCycle>
<contribute>
<source>LOMv1.0</source>
<value>creator</value>
<entity><![CDATA[BEGIN:VCARD
FN: Adamopoulos, Christos
N: Adamopoulos, Christos
"VERSION:3.0"
END:VCARD]]></entity>
</contribute>
<contribute>
<source>LOMv1.0</source>
<value>Scientific Coordinator</value>
<entity><![CDATA[BEGIN:VCARD
FN: Παπαβασιλείου, Αθανάσιος
N: Παπαβασιλείου, Αθανάσιος
"VERSION:3.0"
END:VCARD]]></entity>
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<contribute>
<source>LOMv1.0</source>
<value>Project Executing Organisation</value>
<entity><![CDATA[BEGIN:VCARD
FN: Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)
N: Εθνικό και Καποδιστριακό Πανεπιστήμιο Αθηνών (ΕΚΠΑ)
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<date>
<dateStamp>2013-06-15</dateStamp>
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<string language="el">ECM</string>
</keyword>
<keyword>
<string language="el">Extracellular matrix</string>
</keyword>
<keyword>
<string language="el">Cardiovascular diseases</string>
</keyword>
<keyword>
<string language="el">Atherosclerosis</string>
</keyword>
<keyword>
<string language="el">Cells</string>
</keyword>
<keyword>
<string language="el">Advanced Glycation End-products (AGEs)</string>
</keyword>
<keyword>
<string language="el">Μικροβιολογία</string>
</keyword>
<keyword>
<string language="el">Μοριακή βιολογία</string>
</keyword>
<keyword>
<string language="el">Γλυκοζυλίωση</string>
</keyword>
<keyword>
<string language="el">Κύτταρα</string>
</keyword>
<keyword>
<string language="el">Ωοθήκες</string>
</keyword>
<keyword>
<string language="el">Ενδοθήλιο</string>
</keyword>
</classification>
<technical>
</technical>
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<size>3088325</size>
<format>application/pdf</format>
<location>http://repository.edulll.gr/edulll/bitstream/10795/3400/2/3400_1.68_%ce%91%ce%9d_15_6_13.pdf</location>
</technical>
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<catalog>URI</catalog>
<entry>http://hdl.handle.net/10795/3400</entry>
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<entity><![CDATA[BEGIN:VCARD
FN:National Documentation Centre - National Hellenic Research Foundation
N:National Documentation Centre - National Hellenic Research Foundation
"VERSION:3.0"
END:VCARD]]></entity>
<role><source>LOMv1.0</source><value>creator</value></role>
<date><dateTime>2016-05-25T10:11:22Z</dateTime></date>
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<contribute>
<entity><![CDATA[BEGIN:VCARD
FN:National Documentation Centre - National Hellenic Research Foundation
N:National Documentation Centre - National Hellenic Research Foundation
"VERSION:3.0"
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<role><source>LOMv1.0</source><value>validator</value></role>
<date><dateTime>2016-05-25T10:11:22Z</dateTime></date>
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<metadataSchema>LOMv1.0</metadataSchema>
<language>gre</language>
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<cost>no</cost>
<copyright>no</copyright>
<description>Copyright EYD-EPEDBM (Operational Programme "Education and Lifelong Learning")</description>
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