کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8455132 | 1547998 | 2017 | 16 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Dissecting the CD93-Multimerin 2 interaction involved in cell adhesion and migration of the activated endothelium
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کلمات کلیدی
ECMHUVECC1qRPNHDFAngiogenesis - آنژیوژنزELISA - تست الیزاEnzyme-linked immunosorbent assay - تست الیزاHuman umbilical vein endothelial cell - سلول اندوتلیالی ورید ناقل انسانیEndothelial cell - سلول های اندوتلیالConditioned medium - شرایط محیطیNormal human dermal fibroblast - فیبروبلاست طبیعی پوستی انسانExtracellular matrix - ماتریکس خارج سلولیBag - کیسه
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The glycoprotein CD93 has recently been recognized to play an important role in the regulation of the angiogenic process. Moreover, CD93 is highly expressed in the endothelial cells of tumor blood vessel and faintly expressed in the non-proliferating endothelium. Much evidence suggests that CD93 mediates adhesion in the endothelium. Here we identify Multimerin 2 (MMRN2), a pan-endothelial extracellular matrix protein, as a specific ligand for CD93. We found that CD93 and MMRN2 are co-expressed in the blood vessels of various human tumors. Moreover, disruption of the CD93-MMRN2 interaction reduced endothelial cell adhesion and migration, making the interaction of CD93 with MMRN2 an ideal target to block pathological angiogenesis. Model structures and docking studies served to envisage the region of CD93 and MMRN2 involved in the interaction. Site-directed mutagenesis identified different residue hotspots either directly or indirectly involved in the binding. We propose a molecular model in which the coiled-coil domain of MMRN2 is engaged by F238 of CD93. Altogether, these studies identify the key interaction surfaces of the CD93-MMRN2 complex and provide a framework for exploring how to inhibit angiogenesis by hindering the CD93-MMRN2 interaction.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Matrix Biology - Volume 64, December 2017, Pages 112-127
Journal: Matrix Biology - Volume 64, December 2017, Pages 112-127
نویسندگان
Federico Galvagni, Federica Nardi, Ottavia Spiga, Alfonso Trezza, Giulia Tarticchio, Rosanna Pellicani, Eva Andreuzzi, Elena Caldi, Paolo Toti, Gian Marco Tosi, Annalisa Santucci, Renato V. Iozzo, Maurizio Mongiat, Maurizio Orlandini,