Figure 6.
Figure 6. H-2g–induced angiogenesis in vivo occurs mainly through NFκB and also through JAK2 and PI3K. Matrigel with H-2g and test substance was injected into C57/BL6 mice, and 7 to 10 days later the plugs were removed, homogenized, and hemoglobin was measured. (A) AG490 (50 μM) resulted in 100% inhibition of H-2g–induced hemoglobin production and LY294002 (20 μM) inhibited 92% of H-2g–induced hemoglobin production. (B) We incorporated decoy or antisense (□) and scrambled or sense (▪) ODNs (10 μg/mL) in the Matrigel together with 1 μM H-2g, and results were consistent with the chemical inhibitor effect. JAK2 and PI3K antisense ODNs inhibited blood vessel growth by 70% and 63%, respectively. Incorporating NFκB decoy ODN resulted in 90% inhibition of blood vessel growth compared with incorporation of NFκB scrambled ODN. Results are expressed as the mean of hemoglobin (g/dL) per plug (mg) plus or minus SEM from 6 mice. *Represents a significant difference (P < .05) between the respective groups.

H-2g–induced angiogenesis in vivo occurs mainly through NFκB and also through JAK2 and PI3K. Matrigel with H-2g and test substance was injected into C57/BL6 mice, and 7 to 10 days later the plugs were removed, homogenized, and hemoglobin was measured. (A) AG490 (50 μM) resulted in 100% inhibition of H-2g–induced hemoglobin production and LY294002 (20 μM) inhibited 92% of H-2g–induced hemoglobin production. (B) We incorporated decoy or antisense (□) and scrambled or sense (▪) ODNs (10 μg/mL) in the Matrigel together with 1 μM H-2g, and results were consistent with the chemical inhibitor effect. JAK2 and PI3K antisense ODNs inhibited blood vessel growth by 70% and 63%, respectively. Incorporating NFκB decoy ODN resulted in 90% inhibition of blood vessel growth compared with incorporation of NFκB scrambled ODN. Results are expressed as the mean of hemoglobin (g/dL) per plug (mg) plus or minus SEM from 6 mice. *Represents a significant difference (P < .05) between the respective groups.

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