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. Author manuscript; available in PMC: 2010 Sep 29.
Published in final edited form as: Circulation. 2009 Sep 14;120(13):1255–1265. doi: 10.1161/CIRCULATIONAHA.109.873695

Figure 4. Thrombocytopenic Mac-1-deficient mice remain resistant to TGN. Mac-1 interaction with platelet GpIbα promotes thrombosis.

Figure 4

(A) TGN was induced in WT or Mac-1-/- mice treated with Con IgG or anti-GPIbα to immunodeplete platelets. Serum Cr (sCr), BUN, and LDH were significantly elevated only in thrombocytopenic WT mice following induction of TGN. Thrombocytopenic Mac-1-/- mice exhibited no increase in indices of renal failure following induction of TGN. (B-C) TGN was induced in wild-type mice treated with a polyclonal anti-M2 (αM2) or rabbit IgG control (Con). (B) PAS deposition (left panel) and neutrophil accumulation (right panel) were evaluated in renal tissue. A significant reduction in PAS deposition but no decrease in glomerular neutrophil accumulation was observed in anti-M2 versus IgG control animals. (C) Indices of renal failure including sCr, BUN and LDH were reduced in anti-M2 treated animals compared to Control. Data represent the mean + SEM. *P<0.05 compared with wild-type.