Fig 2: Integrin ß1 deletion downregulated Kindlin-2 and TGFß receptor 2 expression. (A) Cell lysate (30 µg/lane) from integrin ß1 expressing MIA PaCa-2 and integrin ß1 KO clones are immunoblotted for kindlin-2. Normalized protein expression with GAPDH shows a decrease in kindlin-2 expression in clones compared to the normal MIA PaCa-2 cells. (B) The mRNA expression quantified by RT-PCR analysis shows a significant decrease in the expression of kindlin-2 by the deletion of integrin ß1. (C) Lysates were immune blotted with antibody recognizing TGFß receptor 2. GAPDH is used as the loading control. Normalized protein expression shows downregulation of TGFß receptor 2. (D) The mRNA expression quantified by RT-PCR analysis shows a significant decrease in the expression of TGFß receptor 2 by the deletion of integrin ß1. One-way ANOVA was performed by Bonferroni’s test to compare integrin ß1 expressing MIA PaCa-2 and integrin ß1 KO clones indicate a statistically significant difference n = 3, * WT and Clone 2 p < 0.001; # WT and Clone 4 p < 0.001. Quantification is expressed as mean ± SEM.

Fig 3: Irisin attenuates hepatic I/R injury via a kindlin-2 dependent mechanism in steatotic liver. HFD exaggerated I/R-induced liver injury and ROS production. And irisin administration attenuated liver injury, improved mitochondrial function, and reduced oxidative and ER stress in HFD-fed hepatic I/R mice. However, inhibition of kindlin-2 by RNAi eliminated irisin's effects on apoptosis, mitochondrial function, oxidative and ER stress in cultured hepatocytes