Anti-neuropilin-1 peptide inhibits synoviocyte survival, angiogenesis, and experimental arthritis. (Articolo in rivista)

Type
Label
  • Anti-neuropilin-1 peptide inhibits synoviocyte survival, angiogenesis, and experimental arthritis. (Articolo in rivista) (literal)
Anno
  • 2010-01-01T00:00:00+01:00 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#doi
  • 10.1002/art.27243 (literal)
Alternative label
  • Kong JS, Yoo SA, Kim JW, Yang SP, Chae CB, Tarallo V, De Falco S, Ryu SH, Cho CS, Kim WU. (2010)
    Anti-neuropilin-1 peptide inhibits synoviocyte survival, angiogenesis, and experimental arthritis.
    in Arthritis and rheumatism; Wiley-Liss, New York (Stati Uniti d'America)
    (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#autori
  • Kong JS, Yoo SA, Kim JW, Yang SP, Chae CB, Tarallo V, De Falco S, Ryu SH, Cho CS, Kim WU. (literal)
Pagina inizio
  • 179 (literal)
Pagina fine
  • 190 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#url
  • http://onlinelibrary.wiley.com/doi/10.1002/art.27243/abstract (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroVolume
  • 62 (literal)
Rivista
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#note
  • PMID: 20039409 (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#numeroFascicolo
  • 1 (literal)
Note
  • ISI Web of Science (WOS) (literal)
Http://www.cnr.it/ontology/cnr/pubblicazioni.owl#affiliazioni
  • 1. Catholic Univ Korea, Suwon 442723, South Korea 2. Pohang Univ Sci & Technol, Pohang, South Korea 3. Konkuk Univ, Seoul, South Korea 4. Institute of Genetics and Biophysics, CNR, I-80125 Naples, Italy (literal)
Titolo
  • Anti-neuropilin-1 peptide inhibits synoviocyte survival, angiogenesis, and experimental arthritis. (literal)
Abstract
  • Objective. 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. Methods. VEGF(111-165) peptide, which encompasses the NP-1 binding domain of VEGF(165), was generated by cleaving VEGF(165) with plasmin. The effect of this peptide on the interaction between VEGF(165) and its receptor was determined by (125)I-VEGFR binding assay. Assays to determine synoviocyte apoptosis, adhesion, and migration were performed in the presence of VEGF(165) and/ or the peptide. VEGF(165)-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. Results. VEGF(111-165) peptide specifically inhibited the binding of (125)I-VEGF(165) to NP-1 on rheumatoid synoviocytes and ECs. The peptide eliminated the VEGF(165)-mediated increase in synoviocyte survival and activation of p-ERK and Bcl-2. The peptide also completely inhibited a VEGF(165)-induced increase in synoviocyte adhesion and migration. In addition, the anti-NP-1 peptide blocked VEGF(165)-stimulated proliferation, capillary tube formation, and wounding migration of ECs in vitro. VEGF(165)-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. Conclusion. Anti-NP-1 peptide suppressed VEGF(165)-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. (literal)
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