Figure 5
Figure 5. Pericyte-induced expression of survival genes in ECs requires NF-κB activity. (A,B) Expression of target genes of the transcription factor NF-κB was modulated in ECs from tumors in a pericyte-dependent manner, as assessed by quantitative RT-PCR on purified ECs from PNET from RIP1-Tag2 mice treated with control or imatinib (A), and from B16/mock or B16/PDGFB tumors (B). *P < .05 vs control; *P < .01 vs control. (C,D) The NF-κB inhibitor TPCK (3μM) reduced the basal expression of Bcl-w and VEGF-A in MS1 ECs (D) and sensitized MS1 cells to the action of vinblastine (50 ng/mL; D). *P < .05 vs DMSO; **P < .01 vs vinblastine; ***P < .001 vs control. (E,F) Pericytes are unable to modulate the expression of Bcl-w (E) or VEGF-A (F) in ECs on expression of the IκB-α super-repressor protein in MS1 cells. ***P < .001 vs coculture. HBVP indicates human brain vascular pericytes.

Pericyte-induced expression of survival genes in ECs requires NF-κB activity. (A,B) Expression of target genes of the transcription factor NF-κB was modulated in ECs from tumors in a pericyte-dependent manner, as assessed by quantitative RT-PCR on purified ECs from PNET from RIP1-Tag2 mice treated with control or imatinib (A), and from B16/mock or B16/PDGFB tumors (B). *P < .05 vs control; *P < .01 vs control. (C,D) The NF-κB inhibitor TPCK (3μM) reduced the basal expression of Bcl-w and VEGF-A in MS1 ECs (D) and sensitized MS1 cells to the action of vinblastine (50 ng/mL; D). *P < .05 vs DMSO; **P < .01 vs vinblastine; ***P < .001 vs control. (E,F) Pericytes are unable to modulate the expression of Bcl-w (E) or VEGF-A (F) in ECs on expression of the IκB-α super-repressor protein in MS1 cells. ***P < .001 vs coculture. HBVP indicates human brain vascular pericytes.

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