Fig. 3: Targeted knockdown of NPM in mouse hepatic stellate cells (HSCs) significantly inhibited the progression of hepatic fibrosis in mouse models induced by carbon tetrachloride. | Cell Death & Disease

Fig. 3: Targeted knockdown of NPM in mouse hepatic stellate cells (HSCs) significantly inhibited the progression of hepatic fibrosis in mouse models induced by carbon tetrachloride.

From: NPM promotes hepatotoxin-induced fibrosis by inhibiting ROS-induced apoptosis of hepatic stellate cells and upregulating lncMIAT-induced TGF-β2

Fig. 3

A NPM expression of activated HSCs in mouse liver was knocked down by a mouse HSC-specific VA-lip-siRNA complex via tail vein injection. Representative fluorescent images of α-SMA (red) and VA-lip-siRNA-FAM (green) in liver specimens from carbon tetrachloride-treated cirrhotic mice indicated that the VA-lip-siRNA-FAM was specifically enriched in HSC. The mice (n = 5 /group) were injected with VA-lip-siNPM or VA-lip-siNC every 3 days (10 injections in total). The liver specimens were harvested 24 h after the last injection of VA-lip-siRNA-FAM. B Yellow co-location fluorescence of NPM and α-SMA showed that siNPM significantly downregulated NPM expression in HSCs. C Western blot analysis of liver tissues confirmed that NPM was significantly increased in liver. The expression levels of α-SMA, collagen I, and phosphorylated Akt were significantly decreased. D IHC staining and Sirius red staining confirmed that NPM level was significantly decreased by VA-lip-siNPM, and the expressions of markers of liver fibrosis, such as α-SMA and collagen (Sirius red staining), were significantly reduced. E Pearson correlation test showed that NPM was positively correlated with α-SMA and collagen I. Mean ± SEM; **p < 0.01; T test.

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