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. 2010 Sep;177(3):1131–1142. doi: 10.2353/ajpath.2010.091143

Figure 2.

Figure 2

Roles of GPIbα and GPVI in anti-GBM antibody-induced glomerular platelet interactions. A: The role of GPIbα was assessed by comparing glomerular platelet adhesion in mice treated with anti-GBM antibody alone (n = 6) or with the GPIbα inhibitor, alboaggregin-B (280 μg/kg, i.v., n = 3). B: The role of GPVI was determined by comparison of recruitment of platelets from FcRγ chain−/− mice, which lack GPVI, with that of wild-type platelets. Platelets were isolated from either wild-type (n = 6) or FcRγ chain−/− mice (n = 6), and anti-GBM antibody-induced glomerular platelet adhesion assessed as for previous experiments. Data are shown as mean ± SEM. *P < 0.05 versus anti-GBM antibody-treated mice with wild-type platelets.