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. 2002 Apr 15;21(8):1957–1966. doi: 10.1093/emboj/21.8.1957

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Fig. 2. Identification of which integrin is responsible for PDGF-AA-mediated enhanced OP proliferation on Vn. (A) OPs were plated on Vn (10 µg/ml) and the ability of integrin-blocking antibodies and blocking RGD peptides to abolish the PDGF-AA (1 ng/ml)-mediated OP proliferation on Vn was determined, as described in Materials and methods. PDL represents the BrdU incorporation on PDL in the absence of any growth factor. Values shown are means ± SD of at least three independent experiments, each in duplicate. Statistical significance is shown (***P <0.001) between control (Vn + 1 ng/ml PDGF) and any other indicated condition. Note that the PDGF-AA-mediated enhanced OP proliferation on Vn is abolished by anti-integrin β3 and blocking RGD peptides. (B) OPs expressing vector only (VO), the dominant-negative IL2Rβ3 construct or the IL2Rβ1 construct were subjected to proliferation assays on PDL in the presence of 1 ng/ml PDGF-AA, as described in Materials and methods. No significant proliferation is observed in the absence of PDGF (data not shown). Values shown are means ± SD of at least three independent experiments, each in duplicate. Statistical significance is shown (*P <0.05, ***P <0.001) between VO and any other indicated condition. Note the decrease in proliferative capacity of OPs expressing the dominant-negative IL2Rβ3 construct and the increased proliferation of the dominant-negative IL2Rβ1-expressing OPs.