hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-<i>κ</i>B Pathway and VE-Cadherin/<i>β</i>-Catenin Signaling Modulation In Vitro

<div>Effect of hnRNPA2/B1 on the expression of adherens junction molecules in LPS-stimulated HUVECs. HUVECs were transfected with hnRNPA2/B1 siRNA/negative control (NC) siRNA or pcDNA3.1(-)-Myc-6His/pcDNA3.1(-)-hnRNPA2/B1-Myc-6His plasmid for 36 h and then stimulated with 1 <i>μ</i>g/mL LPS for 0, 6, and 12 h. The mRNA and protein were extracted, and VE-cadherin and GAPDH mRNA and protein levels were detected by RT-qPCR and Western blotting, respectively. 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Mediators of Inflammation

fig4

Figure 4

Figure 4: hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-<i>κ</i>B Pathway and VE-Cadherin/<i>β</i>-Catenin Signaling Modulation In Vitro 

Mediators of Inflammation

hnRNPA2/B1 Ameliorates LPS-Induced Endothelial Injury through NF-κB Pathway and VE-Cadherin/β-Catenin Signaling Modulation In Vitro

Figure 4