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Blood, Vol. 109, Issue 10, 4249-4257, May 15, 2007 This Article Abstract Full Text Services Email this article to a friend Alert me to new issues of the journal Rights and Permissions Citing Articles Citing Articles via CrossRef Prolonged shear stress and KLF2 suppress constitutive proinflammatory transcription through inhibition of ATF2 Blood Fledderus et al. 109: 4249 Supplemental materials for: Fledderus et al, Vol 109, Issue 10, 4249-4257 Files in this Data Supplement: Table S1. Expression data (fold change) for genes in cluster groups (PDF, 39.9 KB) - (A) Group A. (B) Group B. (C) Group C. Table S2. Transcription factors with DNA binding sites that are conserved and overrepresented in promoter regions of genes in each of the 3 cluster groups as compared with the whole genome (PDF, 13.1 KB) Figure S1. Shear stress and KLF2 do not modulate ATF2 expression levels (JPG, 33.9 KB) - HUVECs were exposed to prolonged shear stress or were transduced with the lentiviral KLF2 overexpression vector for 5 to 7 days. ATF2 mRNA levels were measured in duplicate by RT-PCR and compared with ATF2 levels in the corresponding static and mock controls. Represented are mean expression levels normalized to expression of ribosomal protein P0 in 3 (shear stress) or 4 (KLF2 overexpression) different HUVEC isolates; ns indicates not significant. Figure S2. KLF2 knockdown increases basal expression of proinflammatory genes (JPG, 82.7 KB) - KLF2 levels in static HUVEC cultures were reduced by 50% by transduction with a lentiviral mock or siKLF2 vector for 4 days (i). Transcription of SELE (ii), CCL2 (iii), IL8 (iv), VCAM1 (v), PAI-1 (vi), and EDN1 (vii) was measured by RT-PCR and represented as the mean normalized to expression of ribosomal protein P0 of 4 different HUVEC isolates. Single asterisks (P < .05) indicate significant difference versus the mock control. This Article Abstract Full Text Services Email this article to a friend Alert me to new issues of the journal Rights and Permissions Citing Articles Citing Articles via CrossRef

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