TNF-α–mediated inhibition of EC migration is enhanced by the loss of MK2 SUMOylation. (A-B) HUVECs were transduced with the appropriate adenoviral constructs (Ad-LacZ, Ad-WT-MK2, Ad-DN-MK2, or Ad-K339R) for 24 hours. Confluent monolayers were “wounded” with a P200 pipette tip and wound closure in the presence or absence of TNF-α (10 ng/mL) was recorded using time-lapse microscopy at 5 different locations per sample for 12 hours with a 30-minute interval. Quantification for the percenthe percentage wound closure can be seen on the right. Note the inhibition by TNF-α on wound closure. Also note the similar effects of Ad-WT-MK2 and Ad-DN-MK2 on enhancing TNF-α–mediated inhibition of wound closure (A). This effect was further enhanced by Ad-MK2-K339R under TNF-α stimulation compared with Ad-WT-MK2 (B). (A-B) Representative images from 1 of 3 independent experiments and quantitative data are shown (n = 3). Values are means ± standard deviation. *P < .05; **P < .01.