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RISS 인기검색어
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- 저자 : Tarallo Valeria (검색결과 2 건)
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Kong, Jin-Sun,Yoo, Seung-Ah,Kim, Jung-Wook,Yang, Seung-Pil,Chae, Chi-Bom,Tarallo, Valeria,Falco, Sandro De,Ryu, Sung-Ho,Cho, Chul-Soo,Kim, Wan-Uk Wiley Subscription Services, Inc., A Wiley Company 2010 Vol.62 No.1
<B>Objective</B><P>To delineate the role of neuropilin-1 (NP-1), a vascular endothelial growth factor receptor (VEGFR), in rheumatoid inflammation and to determine whether blockade of NP-1 could suppress synoviocyte survival and angiogenesis.</P><B>Methods</B><P>VEGF<SUB>111–165</SUB> peptide, which encompasses the NP-1 binding domain of VEGF<SUB>165</SUB>, was generated by cleaving VEGF<SUB>165</SUB> with plasmin. The effect of this peptide on the interaction between VEGF<SUB>165</SUB> and its receptor was determined by <SUP>125</SUP>I-VEGFR binding assay. Assays to determine synoviocyte apoptosis, adhesion, and migration were performed in the presence of VEGF<SUB>165</SUB> and/or the peptide. VEGF<SUB>165</SUB>-induced angiogenesis was assessed by measuring the proliferation, tube formation, and wounding migration of endothelial cells (ECs). Mice were immunized with type II collagen to induce experimental arthritis.</P><B>Results</B><P>VEGF<SUB>111–165</SUB> peptide specifically inhibited the binding of <SUP>125</SUP>I-VEGF<SUB>165</SUB> to NP-1 on rheumatoid synoviocytes and ECs. The peptide eliminated the VEGF<SUB>165</SUB>-mediated increase in synoviocyte survival and activation of p-ERK and Bcl-2. The peptide also completely inhibited a VEGF<SUB>165</SUB>-induced increase in synoviocyte adhesion and migration. In addition, the anti–NP-1 peptide blocked VEGF<SUB>165</SUB>-stimulated proliferation, capillary tube formation, and wounding migration of ECs in vitro. VEGF<SUB>165</SUB>-induced neovascularization in a Matrigel plug in mice was also blocked by treatment with the peptide. Finally, subcutaneous injection of anti–NP-1 peptide suppressed arthritis severity and autoantibody formation in mice with experimental arthritis and inhibited synoviocyte hyperplasia and angiogenesis in arthritic joints.</P><B>Conclusion</B><P>Anti–NP-1 peptide suppressed VEGF<SUB>165</SUB>-induced increases in synoviocyte survival and angiogenesis, and thereby blocked experimental arthritis. Our findings suggest that anti–NP-1 peptide could be useful in alleviating chronic arthritis.</P>
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Cancer-derived exosomal Alu RNA promotes colorectal cancer progression
Magliacane Trotta Sara,Adinolfi Antonio,D’Orsi Luca,Panico Sonia,Mercadante Grazia,Mehlen Patrick,Ambati Jayakrishna,De Falco Sandro,Tarallo Valeria 생화학분자생물학회 2024 Experimental and molecular medicine Vol.56 No.-
Inflammation plays a crucial role in cancer progression, but the relevance of the inflammasome remains unclear. Alu RNA was the first endogenous nucleic acid shown to activate the NLRP3 (nucleotide-binding domain leucine-rich repeat containing 3) inflammasome. Here, we showed that Alu RNA can induce epithelial-to-mesenchymal transition (EMT) through NLRP3 inflammasome activation and IL-1β release in colorectal cancer (CRC) cells. Alu RNA is stored, transported and transferred to CRC cells by exosomes. Exosomal Alu RNA promotes tumorigenesis by inducing invasion, metastasis and EMT via NLRP3 inflammasome activation. Consistent with these data, we found that significantly increased Alu RNA expression correlates with the induction of NLRP3 priming in human CRC patients. Furthermore, the level of Alu RNA in circulating exosomes correlates with CRC progression in a preclinical model. These findings reveal the direct involvement of Alu RNA in cancer pathogenesis, and its presence in CRC cell-derived exosomes could be used as a noninvasive diagnostic biomarker.
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