Knockdown of EVA1A in TNF-stimulated ECs resulted in a trend towards decreased adhesion of monocytes to the endothelium under DF, which, however, did not reach statistical significance ( Figure S7 ), indicating that EVA1A may be priming ECs for monocyte adhesion.
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EVA1A (Eva-1 Homolog A) Promotes Endothelial Apoptosis and Inflammatory Activation Under Disturbed Flow Via Regulation of Autophagy.
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Knockdown of EVA1A resulted in a significant decrease of mRNA levels of E-selectin ( SELE ), VCAM1 , and interleukin 8 ( IL8 ) under DF conditions, whereas there was a nonsignificant trend for decreased expression of ICAM1 (Figure 3 A through 3 D).