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  • 1
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    Del-1, an endogenous leukocyte-endothelial adhesion inhibitor, limits inflammatory cell recruitment (2008)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2008-11-15
    Description: Leukocyte recruitment to sites of infection or inflammation requires multiple adhesive events. Although numerous players promoting leukocyte-endothelial interactions have been characterized, functionally important endogenous inhibitors of leukocyte adhesion have not been identified. Here we describe the endothelially derived secreted molecule Del-1 (developmental endothelial locus-1) as an anti-adhesive factor that interferes with the integrin LFA-1-dependent leukocyte-endothelial adhesion. Endothelial Del-1 deficiency increased LFA-1-dependent leukocyte adhesion in vitro and in vivo. Del-1-/- mice displayed significantly higher neutrophil accumulation in lipopolysaccharide-induced lung inflammation in vivo, which was reversed in Del-1/LFA-1 double-deficient mice. Thus, Del-1 is an endogenous inhibitor of inflammatory cell recruitment and could provide a basis for targeting leukocyte-endothelial interactions in disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2753175/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2753175/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi, Eun Young -- Chavakis, Emmanouil -- Czabanka, Marcus A -- Langer, Harald F -- Fraemohs, Line -- Economopoulou, Matina -- Kundu, Ramendra K -- Orlandi, Alessia -- Zheng, Ying Yi -- Prieto, Darue A -- Ballantyne, Christie M -- Constant, Stephanie L -- Aird, William C -- Papayannopoulou, Thalia -- Gahmberg, Carl G -- Udey, Mark C -- Vajkoczy, Peter -- Quertermous, Thomas -- Dimmeler, Stefanie -- Weber, Christian -- Chavakis, Triantafyllos -- AI067254/AI/NIAID NIH HHS/ -- R01 HL082927/HL/NHLBI NIH HHS/ -- Z01 BC010790-01/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2008 Nov 14;322(5904):1101-4. doi: 10.1126/science.1165218.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Experimental Immunology Branch, Center for Cancer Research, National Cancer Institute (NCI), National Institutes of Health (NIH), Bethesda, MD, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19008446" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bronchoalveolar Lavage Fluid/cytology/immunology ; Carrier Proteins/*physiology ; *Cell Adhesion ; Endothelial Cells/*physiology ; Intercellular Adhesion Molecule-1/metabolism ; Leukocyte Rolling ; Ligands ; Lipopolysaccharides/immunology ; Lung/blood supply/immunology ; Lymphocyte Function-Associated Antigen-1/metabolism ; Mice ; Monocytes/*physiology ; *Neutrophil Infiltration ; Neutrophils/*physiology ; Peritonitis/immunology ; Pneumonia/*immunology ; Recombinant Fusion Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    MicroRNA-92a controls angiogenesis and functional recovery of ischemic tissues in mice (2009)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2009-05-23
    Description: MicroRNAs (miRs) are small noncoding RNAs that regulate gene expression by binding to target messenger RNAs (mRNAs), leading to translational repression or degradation. Here, we show that the miR-17approximately92 cluster is highly expressed in human endothelial cells and that miR-92a, a component of this cluster, controls the growth of new blood vessels (angiogenesis). Forced overexpression of miR-92a in endothelial cells blocked angiogenesis in vitro and in vivo. In mouse models of limb ischemia and myocardial infarction, systemic administration of an antagomir designed to inhibit miR-92a led to enhanced blood vessel growth and functional recovery of damaged tissue. MiR-92a appears to target mRNAs corresponding to several proangiogenic proteins, including the integrin subunit alpha5. Thus, miR-92a may serve as a valuable therapeutic target in the setting of ischemic disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonauer, Angelika -- Carmona, Guillaume -- Iwasaki, Masayoshi -- Mione, Marina -- Koyanagi, Masamichi -- Fischer, Ariane -- Burchfield, Jana -- Fox, Henrik -- Doebele, Carmen -- Ohtani, Kisho -- Chavakis, Emmanouil -- Potente, Michael -- Tjwa, Marc -- Urbich, Carmen -- Zeiher, Andreas M -- Dimmeler, Stefanie -- New York, N.Y. -- Science. 2009 Jun 26;324(5935):1710-3. doi: 10.1126/science.1174381. Epub 2009 May 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Cardiovascular Regeneration, Centre of Molecular Medicine, Goethe-University Frankfurt, 60590 Frankfurt, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/19460962" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis/drug effects ; Down-Regulation ; Endothelial Cells/*metabolism ; Gene Expression Profiling ; Hindlimb/blood supply ; Humans ; Integrin alpha5/genetics/metabolism ; Ischemia/drug therapy/metabolism/pathology/*physiopathology ; Mice ; Mice, Inbred C57BL ; MicroRNAs/antagonists & inhibitors/*metabolism ; Muscle, Skeletal/metabolism ; Myocardial Infarction/metabolism/pathology/*physiopathology ; Myocardium/metabolism ; *Neovascularization, Physiologic ; Oligoribonucleotides/pharmacology/therapeutic use ; RNA, Messenger/genetics/metabolism ; Regional Blood Flow ; Up-Regulation ; Ventricular Function, Left/drug effects ; Zebrafish
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Dietary restriction: standing up for sirtuins (2010)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2010-08-28
    Description: 〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985480/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3985480/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Baur, Joseph A -- Chen, Danica -- Chini, Eduardo N -- Chua, Katrin -- Cohen, Haim Y -- de Cabo, Rafael -- Deng, Chuxia -- Dimmeler, Stefanie -- Gius, David -- Guarente, Leonard P -- Helfand, Stephen L -- Imai, Shin-Ichiro -- Itoh, Hiroshi -- Kadowaki, Takashi -- Koya, Daisuke -- Leeuwenburgh, Christiaan -- McBurney, Michael -- Nabeshima, Yo-Ichi -- Neri, Christian -- Oberdoerffer, Philipp -- Pestell, Richard G -- Rogina, Blanka -- Sadoshima, Junichi -- Sartorelli, Vittorio -- Serrano, Manuel -- Sinclair, David A -- Steegborn, Clemens -- Tatar, Marc -- Tissenbaum, Heidi A -- Tong, Qiang -- Tsubota, Kazuo -- Vaquero, Alejandro -- Verdin, Eric -- P01 AG027916/AG/NIA NIH HHS/ -- R00 AG031182/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG023039/AG/NIA NIH HHS/ -- R01 AG023088/AG/NIA NIH HHS/ -- R01 AG023088-08/AG/NIA NIH HHS/ -- R01 AG024360/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R01 AG028730-05/AG/NIA NIH HHS/ -- R01 HL067724/HL/NHLBI NIH HHS/ -- R01 HL091469/HL/NHLBI NIH HHS/ -- R01 HL102738/HL/NHLBI NIH HHS/ -- R37 AG024360/AG/NIA NIH HHS/ -- Z99 DK999999/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Aug 27;329(5995):1012-3; author reply 1013-4. doi: 10.1126/science.329.5995.1012.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20798296" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*physiology ; Animals ; *Caloric Restriction ; Humans ; *Longevity ; Signal Transduction ; Sirtuins/*physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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