American Society of Hematology

Figure 4

$Figure 4. TIMP-2 modulates VEGF-A–induced VE-cadherin distribution through PKA activity. (A) Quiescent hMVECs were pretreated with forskolin (10μM) or nonhydrolyzable cAMP analog, dibutyryl cAMP (1mM) for 20 minutes and followed by VEGF-A (100 ng/mL) stimulation for 30 minutes. Values represent the mean ± SD of 3 independent experiments. **P < .01, compared with VEGF-A treatment alone. (B) Cells were pretreated with 6-Bnz-cAMP (100μM) or 8-pCPT-2′-O-Me-cAMP, and stimulated with VEGF-A for 30 minutes. The Triton-insoluble or soluble fraction was Western blotted with anti–VE-cadherin antibodies. (C) Cells were pretreated with H89 (20μM) for 20 minutes and followed by Ala + TIMP-2 (100nM) before VEGF-A stimulation for 30 minutes. Integrated density values were obtained and normalized to untreated cells. Results are representative of 3 independent experiments.$

TIMP-2 modulates VEGF-A–induced VE-cadherin distribution through PKA activity. (A) Quiescent hMVECs were pretreated with forskolin (10μM) or nonhydrolyzable cAMP analog, dibutyryl cAMP (1mM) for 20 minutes and followed by VEGF-A (100 ng/mL) stimulation for 30 minutes. Values represent the mean ± SD of 3 independent experiments. **P < .01, compared with VEGF-A treatment alone. (B) Cells were pretreated with 6-Bnz-cAMP (100μM) or 8-pCPT-2′-O-Me-cAMP, and stimulated with VEGF-A for 30 minutes. The Triton-insoluble or soluble fraction was Western blotted with anti–VE-cadherin antibodies. (C) Cells were pretreated with H89 (20μM) for 20 minutes and followed by Ala + TIMP-2 (100nM) before VEGF-A stimulation for 30 minutes. Integrated density values were obtained and normalized to untreated cells. Results are representative of 3 independent experiments.

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