Figure 2
Figure 2. Induction of myocardin transcription and migration in hMSCs by endothelial cells. (A) Quantitative real-time PCR was performed to assess the induction of myocardin in hMSCs by various conditions after 2 days (hMSCs alone, hMSCs cultured with MS1 endothelial cells with contact, hMSCs cultured with MS1 without contact by transwell culture, and hMSCs stimulated with TGFβ1 [10 ng/mL]). Values expressed as fold increase above hMSC-alone levels and normalized by GAPDH. Representative data of 3 separate experiments. (B) Transwell migration assay was performed to assess endothelial cell–induced hMSC migration. Imatinib mesylate at 0.2 μM, 2 μM, and 10 μM was added to test for inhibition of hMSC migration. #P < .001 (medium vs HUVECs); *P < .001 (2 μM imatinib mesylate vs HUVECs); **P < .001 (10 μM imatinib mesylate vs HUVECs).

Induction of myocardin transcription and migration in hMSCs by endothelial cells. (A) Quantitative real-time PCR was performed to assess the induction of myocardin in hMSCs by various conditions after 2 days (hMSCs alone, hMSCs cultured with MS1 endothelial cells with contact, hMSCs cultured with MS1 without contact by transwell culture, and hMSCs stimulated with TGFβ1 [10 ng/mL]). Values expressed as fold increase above hMSC-alone levels and normalized by GAPDH. Representative data of 3 separate experiments. (B) Transwell migration assay was performed to assess endothelial cell–induced hMSC migration. Imatinib mesylate at 0.2 μM, 2 μM, and 10 μM was added to test for inhibition of hMSC migration. #P < .001 (medium vs HUVECs); *P < .001 (2 μM imatinib mesylate vs HUVECs); **P < .001 (10 μM imatinib mesylate vs HUVECs).

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