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. 2011 Apr 29;6(4):e19103. doi: 10.1371/journal.pone.0019103

Figure 1. vGPCR activates VEGF expression through an mTOR-dependent paracrine mechanism.

Figure 1

(A) KS-like lesion developed upon retroviral transduction of vGPCR in TIE2-tva mice (vGPCR tumor), as described in Materials and Methods. (B) H&E and immunohistochemical stainings of vGPCR tumor and human KS, using antibodies against vGPCR, VEGF or an isotype-matched control antibody. (C) Upregulation of VEGF in HMEC1s transfected with Tet REV TA and pBIG AU5 vGPCR and treated with doxycycline (vGPCR), respect to untreated cells (Control). VEGF upregulation in HMEC1 exposed for 2 h or 6 h to supernatants collected from vGPCR-expressing cells (vGPCR CM). (D) Supernatants from vGPCR-expressing cells (vGPCR CM) or control cells (Control CM) were used to treat HMEC1 in the presence or absence of Rapamycin (50 nM). RT-PCR and Western blot analysis were used to determine levels of VEGF mRNA and protein, respectively. (E) EC-vGPCR (10%) were mixed with EC- vCYC/vFLIP (90%), and injected into athymic nu/nu mice for allograft formation. Tumor weight curves, and immunohistochemical detection in tumor tissue of (AU5-tagged) vGPCR-expressing cells, phosphorylated ribosomal S6 protein or VEGF, upon treatment with (10 mg/kg) Rapamycin of vehicle (Control), are shown.