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. Author manuscript; available in PMC: 2020 Feb 15.
Published in final edited form as: Int J Cardiol. 2018 Aug 7;277:212–219. doi: 10.1016/j.ijcard.2018.08.013

Figure 4. DKFZP434I0714 modulates atherorelevant protein genes in human aortic endothelial cells.

Figure 4

(A) Knocking down DKFZP434I0714 in HAEC led to significant transcriptional downregulation of VCAM-1/ICAM-1 and upregulation of eNOS, compared with scramble control. (biological replicates, n=6 in each group; ‡, # and * denotes P <0.05, 0.01 and <0.001, respectively). (B) Immunoblots showed that DKFZP434I0714 knockdown led to significant upregulation of KLF2 and a trend toward increased eNOS proteins in HAEC. The protein expression levels of ICAM-1, VCAM-1 and p-eNOS, however, were not altered by DKFZP434I0714 knockdown (biological replicates, n=3–6 in each group; ‡ denotes P <0.05). (C) Overexpression of DKFZP434I0714 significantly increased transcript expression levels of ICAM-1 and VCAM-1, without affecting eNOS or KLF2, in HAEC (biological replicates, n=3–6 in each group; * denotes P <0.001). (D) Forced expression of DKFZP434I0714, however, did not lead to discernible changes in the protein expression levels of eNOS, ICAM-1, VCAM-1 or KLF2.