We review research on ecological impacts of emerald ash borer (EAB)-induced ash mortality in the Upper Huron River watershed in southeast Michigan near the epicenter of the invasion of North America, where forests have been impacted longer than any others in North America. By 2009, mortality of green, white, and black ash exceeded 99%, and ash seed production and regeneration had ceased. This left an orphaned cohort of saplings too small to be infested, the fate of which may depend on the ability of natural enemies to regulate EAB populations at low densities. There was no relationship between patterns of ash mortality and ash density, ash importance, or community composition. Most trees died over a five-year period, resulting in relatively simultaneous, widespread gap formation. Disturbance resulting from gap formation and accumulation of coarse woody debris caused by ash mortality had cascading impacts on forest communities, including successional trajectories, growth of non-native invasive plants, soil dwelling and herbivorous arthropod communities, and bird foraging behavior, abundance, and community composition. These and other impacts on forest ecosystems are likely to be experienced elsewhere as EAB continues to spread.
Modulation of purinergic signaling, which is critical for vascular homeostasis and the response to vascular injury, is regulated by hydrolysis of proinflammatory ATP and/or ADP by ectonucleoside triphosphate diphosphohydrolase 1 (ENTPD-1; CD39) to AMP, which then is hydrolyzed by ecto-5'-nucleotidase (CD73) to adenosine. We report here that compared with littermate controls (wild type), transgenic mice expressing human ENTPDase-1 were resistant to the formation of an occlusive thrombus after FeCl(3)-induced carotid artery injury. Treatment of mice with the nonhydrolyzable ADP analog, adenosine-5'-0-(2-thiodiphosphate) trilithium salt, Ado-5'-PP[S], negated the protection from thrombosis, consistent with a role for ADP in platelet recruitment and thrombus formation. ENTPD-1 expression decreased whole-blood aggregation after stimulation by ADP, an effect negated by adenosine-5'-0-(2-thiodiphosphate) trilithium salt, Ado-5'-PP[S] stimulation, and limited the ability to maintain the platelet fibrinogen receptor, glycoprotein α(IIb)/β(3), in a fully activated state, which is critical for thrombus formation. In vivo treatment with a CD73 antagonist, a nonselective adenosine-receptor antagonist, or a selective A(2A) or A(2B) adenosine-receptor antagonist, negated the resistance to thrombosis in transgenic mice expressing human ENTPD-1, suggesting a role for adenosine generation and engagement of adenosine receptors in conferring in vivo resistance to occlusive thrombosis in this model. In summary, our findings identify ENTPDase-1 modulation of purinergic signaling as a key determinant of the formation of an occlusive thrombus after vascular injury.
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