Figure 5.
A collaboration between MGL and AMR facilitates binding of desialylated platelets to Kupffer cells.(A) SD-IVM was performed on the liver of control mice, mice treated with ASF, Asgr1−/− mice, wild-type mice treated with MGL1/2 blocking antibody (Ab), and Asgr1−/− mice treated with MGL1/2 blocking antibody after injection of 50 mU sialidase. Kupffer cells and platelets were labeled using anti-F4/80 and anti-CD49b antibodies, respectively. Representative images taken at the indicated time points. Scale bars are 70 µm, except for the WT+MGL1/2 antibody images, where scale bars are 100 µm. (B) Quantification of platelet accumulation shown in A with n ≥ 4 mice per group, normalized to control mice values. Results from all experiments shown are representative of at least three independent experiments.

A collaboration between MGL and AMR facilitates binding of desialylated platelets to Kupffer cells. (A) SD-IVM was performed on the liver of control mice, mice treated with ASF, Asgr1−/− mice, wild-type mice treated with MGL1/2 blocking antibody (Ab), and Asgr1−/− mice treated with MGL1/2 blocking antibody after injection of 50 mU sialidase. Kupffer cells and platelets were labeled using anti-F4/80 and anti-CD49b antibodies, respectively. Representative images taken at the indicated time points. Scale bars are 70 µm, except for the WT+MGL1/2 antibody images, where scale bars are 100 µm. (B) Quantification of platelet accumulation shown in A with n ≥ 4 mice per group, normalized to control mice values. Results from all experiments shown are representative of at least three independent experiments.

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