Figure 3 : Effect of genetic KCa3.1 depletion in CCl4 induced liver fibrosis in mice.

From: The calcium-activated potassium channel KCa3.1 is an important modulator of hepatic injury

Figure 3

KCa3.1−/− mice show increased fibrosis by the evaluation of hepatic hydroxyproline (A) and collagen, as evaluated by Sirius red and fluorescent stain for collagen1 (B,C) compared to wt littermates. These differences were especially pronounced in severe fibrosis, seen after 12 weeks of CCl4 exposure. Similarly, knockouts have higher expression of TGFβ mRNA, and increased inflammatory activity, as evaluated by the higher transcription of the TNFα gene (D). Representative Western blot analysis of the hepatic protein-expression of PCNA, JNK, pJNK, p-c-Src Thr418 and 530 were analysed in fibrotic mice following 12 weeks CCl4 exposure. The hepatic expression of PCNA was higher in KCa3.1−/−. They similarly demonstrated increased pJNK and p-c-SrcThr418 expression, but lower Thr530 (E+F), suggesting a direct effect on c-Src and volume control (E,F).