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. Author manuscript; available in PMC: 2017 Aug 1.
Published in final edited form as: Crit Care Med. 2016 Aug;44(8):e639–e650. doi: 10.1097/CCM.0000000000001629

Fig. 6. KLF2 is a key upstream transcription factor involved in the down-regulation of miR-126a-3p in vascular ECs and arteries in endotoxemia.

Fig. 6

A. Expression of pri-miR-126a-3p in aortas from LPS-injected mice is decreased. n=6; *p<0.05 vs control group. B. Expression of pri-miR-126a-3p in LPS-treated endothelial cells is decreased. n=6; *p<0.05 vs control group. C. Expression of KLF2 protein in aortas from LPS-injected mice is decreased. n=6; *p<0.05 vs control group. D. Expression of KLF2 protein in LPS-treated endothelial cells is decreased. n=6; *p<0.05 vs control group. E. Overexpression of KLF2 via Ad-KLF2 in mouse aortas in vivo. n=6; *p<0.05 vs control group. F. Overexpression of KLF2 via Ad-KLF2 in cultured mouse endothelial cells in vitro. n=6; *p<0.05 vs control group. G. LPS-induced down-regulation of miR-126a-3p in mouse aortas could be efficiently inhibited by KLF2 over-expression via Ad-KLF2 (Fig. 6G and 6H). n=6; *p<0.05 vs Ad-GFP control group. H. LPS-induced down-regulation of miR-126a-3p in mouse ECs could be efficiently inhibited by KLF2 over-expression via Ad-KLF2. =6; *p<0.05 vs Ad-GFP control group.