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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. 5. SPRED1 and VCAM-1 are two direct target genes of miR-126a-3p.

Fig. 5

A. a luciferase reporter construct, containing the putative miR-126a-3p binding sequence from 3′-UTR of the SPRED1 or VCAM-1 mRNA was transfected into HEK293 with vehicle, pDNR-CMV, pmiR-126a-3p . The constructs without the miR-126a-3p binding sequence were used as the truncated controls. pmiR-miR-126a-3p inhibited luciferase activity. In the truncated control group, the inhibitory effect of pmiR-126a-3p disappeared. Note: n=6; *p < 0.05 compared with pDNR-CMV group. B. The effects of miR-126a-3p inhibition or miR-126a-3p overexpression on the protein levels of SPRED1 and VCAM-1 in cultured ECs. Note: n=6; *p < 0.05 compared with oligo control group. C. Representative western blots of SPRED1 and VCAM-1 in ECs with different treatments. D. Increased protein levels of SPRED1 and VCAM-1 in LPS-treated ECs. Note: n=6; *p < 0.05 compared with control group. E. Representative western blots of SPRED1 and VCAM-1 of D. F. Increased protein levels of SPRED1 and VCAM-1 in aortas of LPS-treated mice.Note: n=5; *p < 0.05 compared with control group. G. Representative western blots of SPRED1 and VCAM-1 of F. H. Increased protein levels of SPRED1 and VCAM-1 in skin vessels of patients with sepsis Note: n=5; *p < 0.05 compared with control group. I. Representative western blots of SPRED1 and VCAM-1 of H.