Fig. 1: ProAgio induces apoptosis of activated HSC.
From: Targeting integrin αvβ3 by a rationally designed protein for chronic liver disease treatment
a Expression of integrin αv and β3 in activated (an HSC) and inactivated (q HSC) human primary HSC cells were analyzed by immunoblots using anti-αv (IB: integrin αv) and anti-β3 (IB: integrin β3) antibodies. Immunoblot of GAPDH (IB: GAPDH) is a loading control. b mRNA levels of integrin αv and integrin β3 in activated (an HSC) and inactivated (q HSC) human primary HSC cells were analyzed by RT-PCR. The integrin mRNAs are presented as fold changes by defining the mRNA levels of inactivated HSC as 1. c–e Apoptosis of human primary HSC cells (c), LX-2 cells (d, e) under treatment of indicated concentrations of ProAgio was measured by apoptosis kit. f Co-immunoprecipitations of caspase 8 with integrin β3 (IP:integrin β3) were analyzed by immunoblots (IB:caspase 8). LX-2 cells were treated with ProAgio 5 h prior to the preparation of extracts. Immunoblot of integrin β3 (IB:integrin β3) and IgG (IB:IgG) indicates the amount of β3 and amounts of IgG, which were precipitated down in the co-IPs. c–e Apoptosis was presented as apoptosis (%) by defining buffer treated cells as 0%. a–c Primary HSC cells were activated by culturing 7 days in presence of 5 ng/ml TGF-β (an HSC). Freshly plated cells were regarded as inactivated HSC cells (q HSC). Error bars in b–e are standard deviations of five independent experiments. Statistical significance was calculated by two-tailed unpaired Student’s t test, ***P < 0.001.
