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. Author manuscript; available in PMC: 2016 Jun 10.
Published in final edited form as: Cell Host Microbe. 2015 Jun 10;17(6):775–787. doi: 10.1016/j.chom.2015.05.011

Figure 1. Hla Alters Platelet Aggregation.

Figure 1

(A) von Willebrand factor (red) release from primary human pulmonary artery endothelial cells (HPAECs) was assessed following stimulation with histamine, HlaH35L, Hla, or Hla in the presence of the ADAM10 inhibitor GI254023X or vehicle control DMSO. Dapi (blue) denotes cell nuclei.

(B) Quantification of calcein AM-labeled human platelets that adhere to HlaH35L or Hla-treated HPAECs as in (A), ****p ≤ 0.0001.

(C) Adherence of Hla or HlaH35L-treated calcein AM-labeled platelets to collagen-coated slides.

(D) Toxin-induced metalloprotease activity in platelets stimulated with Hla in the presence of a fluorogenic ADAM10 substrate for 30 min, *p ≤ 0.05.

(E) GPVI immunoblot analysis of lysates prepared from human platelets treated with HlaH35L or Hla. FL, full-length GPVI; NTF, N-terminal GPVI fragment.

(F) Activated GPIIb-IIIa expression on human platelets pre-treated with Hla (black line) or HlaH35L (dotted line) followed by treatment with collagen compared to collagen-alone control (gray line).

(G) Aggregation of calcein AM-labeled platelets on plate-bound human fibrinogen following treatment as in (C). Scale bars, 10 μm. mean ± SD.